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COVID-19 and hepatic injury: cellular and molecular mechanisms in diverse liver cells 被引量:3
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作者 Fares E M Ali Mostafa K Abd El-Aziz +2 位作者 Mahmoud M Ali Osama M Ghogar Adel G Bakr 《World Journal of Gastroenterology》 SCIE CAS 2023年第3期425-449,共25页
The coronavirus disease 2019(COVID-19)represents a global health and economic challenge.Hepatic injuries have been approved to be associated with severe acute respiratory syndrome coronavirus(SARS-CoV-2)infection.The ... The coronavirus disease 2019(COVID-19)represents a global health and economic challenge.Hepatic injuries have been approved to be associated with severe acute respiratory syndrome coronavirus(SARS-CoV-2)infection.The viral tropism pattern of SARS-CoV-2 can induce hepatic injuries either by itself or by worsening the conditions of patients with hepatic diseases.Besides,other factors have been reported to play a crucial role in the pathological forms of hepatic injuries induced by SARS-CoV-2,including cytokine storm,hypoxia,endothelial cells,and even some treatments for COVID-19.On the other hand,several groups of people could be at risk of hepatic COVID-19 complications,such as pregnant women and neonates.The present review outlines and discusses the interplay between SARS-CoV-2 infection and hepatic injury,hepatic illness comorbidity,and risk factors.Besides,it is focused on the vaccination process and the role of developed vac-cines in preventing hepatic injuries due to SARS-CoV-2 infection. 展开更多
关键词 COVID-19 hepatic injury Viral tropism COVID-19 comorbidity VACCINATION
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Ex vivo-expanded bone marrow stem cells home to the liver and ameliorate functional recovery in a mouse model of acute hepatic injury 被引量:16
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作者 Shi-Zhu Jin,Bing-Rong Liu,Jun Xu,Fu-Lai Gao,Zong-Jing Hu,Xin-Hong Wang,Feng-Hua Pei,Yu Hong,Hong-Yan Hu and Ming-Zi Han Department of Gastroenterology and Hepatology,and Department of Science Research Management,Second Affiliated Hospital,Harbin Medical University,Harbin 150080,China Department of Gastroenterology and Hepatology,Fourth Affiliated Hospital,Harbin Medical University,Harbin 150001,China 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2012年第1期66-73,共8页
BACKGROUND:Stem cell transplantation provides a theoretical approach for liver regeneration medicine;it may promote liver regeneration and self-repair.However,the transplantation of bone marrow-mesenchymal stem cells ... BACKGROUND:Stem cell transplantation provides a theoretical approach for liver regeneration medicine;it may promote liver regeneration and self-repair.However,the transplantation of bone marrow-mesenchymal stem cells expanded ex vivo as a therapy for liver disease has rarely been investigated.This study aimed to explore whether bone marrow stem cells expanded ex vivo home to the liver and foster hepatic recovery after CCl 4 injury.METHODS:Bone marrow cells from BALB/c mice were expanded ex vivo by multiple-passage cultivation,characterized by cytoflow immunofluorescence,and pre-labeled with PKH26 before intravenous infusion into animals treated with CCl 4.The integration of bone marrow cells into the liver was examined microscopically,and plasma hepatic enzymes were determined biochemically.RESULTS:Cultured bone marrow cells exhibited antigenic profiles comparable to those of primary medullary stem cells.Double immunofluorescence showed colocalization of these cells with proliferative activity and albumin expression in the liver of CCl 4 -treated mice.Densitometry showed increased in situ cell proliferation (50±14 vs 20±3 cells/high-power field,P<0.05) and albumin expression (149±25 vs 20±5 cells/high-power field,P<0.05) in the liver,as well as reduced serum aminotransferase levels (P<0.05) and better survival rates (P<0.05) in animals receiving cultured bone marrow cells relative to controls.CONCLUSIONS:Ex vivo-expanded bone marrow cells are capable of relocating to and proliferating in the chemically- injured liver.Transplantation of these pluripotent stem cells appears to improve serum indices of liver function and survival rate in mice after CCl4-induced hepatic damage. 展开更多
关键词 stem cell therapy stem cell culture acute hepatic injury
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Dimethylacetamide-induced Hepatic Injury in Vitro: Mechanism and Potential Preventive Strategy 被引量:3
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作者 LIU Xin GONG Wei +1 位作者 XU Yan Qiong ZHU Bao Li 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2016年第2期153-157,共5页
N,N-Dimethylacetamide (DMAc) is a widely used organic solvent in modern chemical industry with low to moderate hepatotoxicity to occupational health of employees. But so far, there are fewer and less conclusive data... N,N-Dimethylacetamide (DMAc) is a widely used organic solvent in modern chemical industry with low to moderate hepatotoxicity to occupational health of employees. But so far, there are fewer and less conclusive data concerning its pathogenic mechanism in detail. In current study, the toxicity of DMAc was firstly investigated on human normal hepatocytes (LO-2), using a series of molecular biology measurements to ananlyze the effect and mechanism of DMAc-induced hepatic cell injury and explore effective prophylactic measures. We found that DMAc triggered LO-2 apoptosis in a obviously dose-dependent manner, caused by increased ROS generation and activation of Bcl-2 pathway. Significantly, glutathione (GSH) rather than vitamin C (Vit C) could partially inhibit DMAc-induced apoptosis thus showing potential as a effective precaution for workers. 展开更多
关键词 GSH Figure Dimethylacetamide-induced hepatic injury in Vitro Mechanism and Potential Preventive Strategy 33258 NAC
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The new antioxidant 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2- dihydroquinoline has a protective effect against carbon tetrachloride-induced hepatic injury in rats
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作者 Evgenii Dmitrievich Kryl'skii Darya Andreevna Sinitsyna +4 位作者 Tatyana Nikolaevna Popova Khidmet Safarovich Shikhaliev Svetlana Mikhajlovna Medvedeva Larisa Vladimirovna Matasova Valentina Olegovna Mittova 《The Journal of Biomedical Research》 CAS CSCD 2022年第6期423-434,共12页
Liver diseases with the central pathogenetic mechanism of oxidative stress are one of the main causes of mortality worldwide.Therefore,dihydroquinoline derivatives,which are precursors of hepatoprotectors and have ant... Liver diseases with the central pathogenetic mechanism of oxidative stress are one of the main causes of mortality worldwide.Therefore,dihydroquinoline derivatives,which are precursors of hepatoprotectors and have antioxidant activity,are of interest.We have previously found that some compounds in this class have the ability to normalize redox homeostasis under experimental conditions.Here,we initially analyzed the hepatoprotective potential of the dihydroquinoline derivative 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline(BHDQ)for carbon tetrachloride(CCl4)-induced liver injury in rats.Results suggested that BHDQ normalized the alanine aminotransferase,aspartate aminotransferase,and gamma-glutamyl transpeptidase in serum.We also observed an improvement in liver tissue morphology related to BHDQ.Animals with CCl4-induced liver injuries treated with BHDQ had less oxidative stress compared to animals with CCl4-induced liver injury.BHDQ promoted activation changes in superoxide dismutase,catalase,glutathione peroxidase,glutathione reductase,and glutathione transferase on control values in animals with CCl4-induced liver injury.BHDQ also activated gene transcription in Sod1 and Gpx1 via nuclear factor erythroid 2-related factor 2 and forkhead box protein O1 factors.Therefore,the compound of concern has a hepatoprotective effect by inhibiting the development of necrotic processes in the liver tissue,through antioxidation. 展开更多
关键词 CCl4-induced hepatic injury oxidative stress 1-benzoyl-6-hydroxy-2 2 4-trimethyl-1 2-dihydroquinoline antioxidants
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Curcumin protects against acetaminophen-induced apoptosis in hepatic injury 被引量:5
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作者 Gang Li Jun-Bao Chen +5 位作者 Chao Wang Zhi Xu Hao Nie Xiao-Yan Qin Xiao-Mei Chen Quan Gong 《World Journal of Gastroenterology》 SCIE CAS 2013年第42期7440-7446,共7页
AIM:To explore the effects of curcumin(CMN)on hepatic injury induced by acetaminophen(APAP)in vivo.METHODS:Male mice were randomly divided into three groups:groupⅠ(control)mice received the equivalent volumes of phos... AIM:To explore the effects of curcumin(CMN)on hepatic injury induced by acetaminophen(APAP)in vivo.METHODS:Male mice were randomly divided into three groups:groupⅠ(control)mice received the equivalent volumes of phosphate-buffered saline(PBS)intraperitoneally(ip);GroupⅡ[APAP+carboxymethylcellulose(CMC)]mice received 1%CMC(vehicle)2h before APAP injection;GroupⅢ(APAP+CMN)mice received curcumin(10 or 20 mg/kg,ip)2 h before before or after APAP challenge.In GroupsⅡandⅢ,APAP was dissolved in pyrogen-free PBS and injected at a single dose of 300 mg/kg.CMN was dissolved in 1%CMC.Mice were sacrificed 16 h after the APAP injection to determine alanine aminotransferase(ALT)levels in serum and malondialdehyde(MDA)accumulation,superoxide dismutase(SOD)activity and hepatocyte apoptosis in liver tissues.RESULTS:Both pre-and post-treatment with curcumin resulted in a significant decrease in serum ALT compared with APAP treatment group(10 mg/kg:801.46±661.34 U/L;20 mg/kg:99.68±86.48 U/L vs 5406.80±1785.75 U/L,P<0.001,respectively).The incidence of liver necrosis was significantly lowered in CMN treated animals.MDA contents were significantly reduced in 20 mg/kg CMN pretreatment group,but increased in APAP treated group(10.96±0.87 nmol/mg protein vs 16.03±2.58 nmol/mg protein,P<0.05).The decrease of SOD activity in APAP treatment group and the increase of SOD in 20 mg/kg CMN pretreatment group were also detected(24.54±4.95 U/mg protein vs 50.21±1.93 U/mg protein,P<0.05).Furthermore,CMN treatment efficiently protected against APAPinduced apoptosis via increasing Bcl-2/Bax ratio.CONCLUSION:CMN has significant therapeutic potential in both APAP-induced hepatotoxicity and other types of liver diseases. 展开更多
关键词 ACETAMINOPHEN Acute hepatic injury Apoptosis Free RADICALS CURCUMIN
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Naringenin protects against isoniazid- and rifampicininduced apoptosis in hepatic injury 被引量:5
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作者 Chao Wang Rui-Qin Fan +2 位作者 Yan-Xiang Zhang Hao Nie Kan Li 《World Journal of Gastroenterology》 SCIE CAS 2016年第44期9775-9783,共9页
AIM To explore the protective effects and mechanisms of naringenin(NRG) on hepatic injury induced by isoniazid(INH) and rifampicin(RIF).METHODS Male mice were randomly divided into four groups and treated for 14 d as ... AIM To explore the protective effects and mechanisms of naringenin(NRG) on hepatic injury induced by isoniazid(INH) and rifampicin(RIF).METHODS Male mice were randomly divided into four groups and treated for 14 d as follows: normal control group was administered intragastrically with normal saline solution alone; model group was administered intragastrically with INH(100 mg/kg) and RIF(100 mg/kg); lowand high-dosage NRG pretreatment groups were administered intragastrically with different doses of NRG(50 or 100 mg/kg) 2 h before INH and RIF challenge. Mice were killed 16 h after the last dose of drug treatment to determine activity of serum transaminases. Oxidative stress was evaluated by measuring hepatic glutathione(GSH) and superoxide dismutase(SOD) and malondialdehyde(MDA) levels. Histopathological changes in hepatic tissue were observed under the optical microscope. Hepatocyte apoptosis was measured by TUNEL assay and caspase-3 activation. Expression of Bcl-2 and Bax in liver was determined by western blot.RESULTS Both low- and high-dosage NRG pretreatment obviously alleviated serum levels of alanine aminotransferase and aspartate aminotransferase, liver index, hepatic MDA content, and increased hepatic GSH content and SOD activity compared with the INH and RIF-treated group(44.71 ± 8.15 U/L, 38.22 ± 6.64 U/L vs 58.15 ± 10.54 U/L; 98.36 ± 14.78 U/L, 92.41 ± 13.59 U/L vs 133.05 ± 19.36 U/L; 5.34% ± 0.26%, 4.93% ± 0.25% vs 5.71% ± 0.28%; 2.76 ± 0.67 nmol/mgprot, 2.64 ± 0.64 nmol/mgprot vs 4.49 ± 1.12 nmol/mgprot; 5.91 ± 1.31 mg/gprot, 6.42 ± 1.42 mg/gprot vs 3.11 ± 0.73 mg/gprot; 137.31 ± 24.62 U/mgprot, 148.83 ± 26.75 U/mgprot vs 102.34 ± 19.22 U/mgprot; all P < 0.01 or 0.05). Histopathological evaluation showed obvious necrosis and inflammatory cell infiltration in liver of mice administered INH and RIF; however, mice pretreated with NRG showed minor hepatic injury. In addition, INH and RIF resulted in hepatocyte apoptosis, and NRG pretreatment dramatically suppressed INHand RIF-induced hepatocytes apoptosis. Furthermore, NRG-mediated anti-apoptotic effects seemed to be in connection with its regulation of Bax and Bcl-2 protein expression in hepatic tissue.CONCLUSION NRG might attenuate INH- and RIF-induced hepatic injury via suppression of oxidative stress and hepatocyte apoptosis. 展开更多
关键词 NARINGENIN ISONIAZID RIFAMPICIN OXIDATIVE stress Apoptosis hepatic injury
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Early activated hepatic stellate cell-derived molecules reverse acute hepatic injury 被引量:2
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作者 Wen-Ju Chang Lu-Jun Song +7 位作者 Tuo Yi Kun-Tang Shen Hong-Shan Wang Xiao-Dong Gao Min Li Jian-Min Xu Wei-Xin Niu Xin-Yu Qin 《World Journal of Gastroenterology》 SCIE CAS 2015年第14期4184-4194,共11页
AIM: To test whether hepatic stellate cells(HSCs) at different activation stages play different roles in acetaminophen(APAP)-induced acute liver injury(ALI).METHODS: HSCs were isolated from mouse liver and cultured in... AIM: To test whether hepatic stellate cells(HSCs) at different activation stages play different roles in acetaminophen(APAP)-induced acute liver injury(ALI).METHODS: HSCs were isolated from mouse liver and cultured in vitro.Morphological changes of initiation HSCs [HSCs(5d)] and perpetuation HSCs [HSCs(p3)] were observed by immunofluorescence and transmission electron microscopy.The protective effects of HSCderived molecules, cell lysates and HSC-conditioned medium(HSC-CM) were tested in vivo by survival and histopathological analyses.Liver injury was determined by measuring aminotransferase levels in the serum and by histologic examination of tissue sections under a light microscope.Additionally, to determine the molecular mediators of the observed protective effects of initiation HSCs, we examined HSC-CM using a highdensity protein array.RESULTS: HSCs(5d) and HSCs(p3) had different morphological and phenotypic traits.HSCs(5d) presented a star-shaped appearance with expressing α-SMA at non-uniform levels between cells.However, HSCs(p3) evolved into myofibroblast-like cells without lipid droplets and expressed a uniform and higher level of α-SMA.HSC-CM(5d), but not HSC-CM(p3), provided a significant survival benefit and showed a dramatic reduction of hepatocellular necrosis and panlobular leukocyte infiltrates in mice exposed to APAP.However, this protective effect was abrogated at higher cell masses, indicating a therapeutic window of effectiveness.Furthermore, the protein array screenrevealed that HSC-CM(5d) was composed of many chemokines and growth factors that correlated with inflammatory inhibition and therapeutic activity.When compared with HSC-CM(p3), higher levels of monocyte chemoattractant protein-1, macrophage inflammatory protein-1γ, hepatocyte growth factor, interleukin-10, and matrix metalloproteinase-2, but lower levels of stem cell factor and Fas-Ligand were observed in HSCCM(5d).CONCLUSION: These data indicated that initiation HSCs and perpetuation HSCs were different in morphology and protein expression, and provided the first experimental evidence of the potential medical value of initiation HSC-derived molecules in the treatment of ALI. 展开更多
关键词 hepatic stellate cells Acute liver injury Initiati
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Kupffer cells contribute to concanavalin A-induced hepatic injury through a Th1 but not Th17 type response-dependent pathway in mice 被引量:2
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作者 Lin Chen,Xiao-Jun Xie,Yu-Fu Ye,Lin Zhou,Hai-Yang Xie,Qin-Fen Xie, Jiong Tian and Shu-Sen ZhengZhejiang University School of Medicine,Hangzhou 310003,ChinaKey Laboratory of Combined Multi-organ Transplantation,Ministry of Public Health Department of Hepatobiliary and Pancreatic Surgery Department of Nephrology,First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2011年第2期171-178,共8页
BACKGROUND:Increasing evidence suggests that a close interaction of Kupffer cells with T cells plays a central role in concanavalin A-induced hepatic injury in mice,but the underlying mechanisms remain obscure.The pre... BACKGROUND:Increasing evidence suggests that a close interaction of Kupffer cells with T cells plays a central role in concanavalin A-induced hepatic injury in mice,but the underlying mechanisms remain obscure.The present study aimed to determine the relative roles of Th1 and Th17 type responses in concanavalin A-induced hepatic injury in mice, and to investigate whether or not Kupffer cells contribute to hepatic injury via a Th1 or Th17 type response-dependent pathway. METHODS:Immune-mediated hepatic injury was induced in C57BL/6 mice by intravenous injection of concanavalin A. Kupffer cells were inactivated by pretreatment with gadolinium chloride 24 hours before the concanavalin A injection.The interferon-gamma(IFN-γ)and interleukin-17(IL-17)pathways were blocked by specific neutralizing antibodies.Hepatic injury was assessed using serum transferase activity and pathological analysis.Expression of inflammatory cytokines within the liver was detected by real-time polymerase chain reaction and immunohistochemistry. RESULTS:Neutralization of IFN-γsignificantly attenuated concanavalin A-induced hepatic injury.However,neutralization of IL-17 failed to suppress the injury.Inactivation of Kupffer cells by gadolinium chloride pretreatment protected against concanavalin A-induced injury and significantly reduced hepatic cytokine levels including TNF-α,IL-6 and IFN-γbut not IL-17.CONCLUSION:Our findings suggest that Kupffer cells contribute to concanavalin A-induced hepatic injury via a Th1 type response-dependent pathway and production of inflammatory cytokines including TNF-α,IL-6 and IFN-γ. 展开更多
关键词 Kupffer cells INTERFERON-GAMMA INTERLEUKIN-17 concanavalin A hepatic injury hepatITIS
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Propolis modulates cellular biochemistry, antioxidants, cytokine profile, histological and ultra-morphological status against antituberculosis drugs induced hepatic injury 被引量:1
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作者 Nisha Sahu Gita Mishra +2 位作者 Hemeshwer Kumar Chandra Satendra Kumar Nirala Monika Bhadauria 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2018年第11期609-620,共12页
To evaluate hepatic injury induced by antituberculosis drugs(ATDs) when administered orally for 2, 4, 6 and 8 weeks and the therapeutic potential of propolis(bee hive product) against ATDs induced hepatic injury. Meth... To evaluate hepatic injury induced by antituberculosis drugs(ATDs) when administered orally for 2, 4, 6 and 8 weeks and the therapeutic potential of propolis(bee hive product) against ATDs induced hepatic injury. Methods: The ATDs were administered for 8 weeks as well as propolis extract at three different doses(100, 200, 400 mg/kg) conjointly for 8 weeks in rats. Silymarin(50 mg/kg) was given as positive control. Animals were euthanized after 8 weeks; blood and liver samples were collected to perform various biochemicals, serological and histopathological and ultramorphological studies. Results: Significant increase(P < 0.05) in aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, triglyceride and cholesterol along with reduction in glucose and albumin level were noted after ATDs induced hepatic injury. Significant increase(P < 0.05) in lipid peroxidation, triglyceride, cholesterol and CYP2E1 activity; decline in reduced glutathione, catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase, glucose-6-phosphatase dehydrogenase activity were observed after ATDs intoxication. Due to presence of a wide range of flavonoids and polyphenols in propolis extract, its administration reduced hepatic injury and maintained biochemical indices towards control. Histopathological and electron microscopic observations indicated hepatoprotective potential of propolis at cellular level whereas, TNF-α, IL-6 and IGF-1 confirmed therapeutic potential of propolis at molecular level. Conclusions: It can be concluded that propolis possess hepatoprotective potential against ATDs induced hepatic injury that may prove itself as a clinically useful natural product in management of drug induced liver injury. 展开更多
关键词 ANTITUBERCULOSIS drugs PROPOLIS Biochemical hepatic injury
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Induction of acute hepatic injury by endotoxin in mice 被引量:3
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《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2002年第4期558-564,共7页
Objective: To investigate the changes of scavenger re-ceptor (SR) and CD<sub>14</sub> in Kupffer cells in endotox-emia in order to uncover the mechanism of the liverto turn a defense organ into effector ... Objective: To investigate the changes of scavenger re-ceptor (SR) and CD<sub>14</sub> in Kupffer cells in endotox-emia in order to uncover the mechanism of the liverto turn a defense organ into effector one in sepsis.Methods: Mouse models of endotoxemia of differentseverity were reproduced by injection of different do-ses of lipopolysaccharide (LPS) via the tail vein.The expression of SR and CD<sub>14</sub> in the liver was as-sayed by immunohistochemistry and was subsequent-ly analyzed with an image analysis system. The levelsof TNF-α and IL-6 in liver tissue were determinedwith ELISA.Results: The expression of SR in the liver in the high-dose group was markedly decreased one hour afterinjection of LPS, and also in the low-dose group at 3hours. The expression of SR in the liver in the twogroups was shown to be progressively decreased withthe time prolonged. There was significant differencein average optical density (OD) values of SR be-tween the two groups. The expression of CD<sub>14</sub> in thetwo groups was shown to be significantly increasedone hour after injection of LPS, and more signifi-cantly with the time prolonged. But there was no sig-nificant difference in OD values of CD<sub>14</sub> between thetwo groups. The contents of intrahepatic proinflam-matory mediators TNF-α, IL-6, ALT and TBILwere significantly increased after injection of LPS.Correlation analysis revealed that the changes ofTNF-α, IL-6, ALT, and TBIL were negatively cor-related with the expression of SR, and positively withthe expression of CD<sub>14</sub>.Conclusion: The up-regnlation of CD<sub>14</sub> expressionand down-regulation of SR expression on Kupffercells might be one of the important mechanisms forthe conversion of Kupffer cells from immune defen-sive to inflammatory response cells in acute hepaticinjury. 展开更多
关键词 hepatic injury ENDOTOXEMIA SCAVENGER receptor CD14 tumor NECROSIS factor-α INTERLEUKIN
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Effect of naked eukaryotic expression plasmid encoding rat augmenter of liver regeneration on acute hepatic injury and hepatic failure in rats 被引量:10
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作者 Li-MeiZhang Dian-WuLiu +4 位作者 Jian-BoLiu Xiao-LinZhang Xiao-BoWang Long-MeiTang Li-QinWang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第24期3680-3685,共6页
AIM: To study the protective effect of eukaryotic expression plasmid encoding augmenter of liver regeneration (ALR) on acute hepatic injury and hepatic failure in rats. METHODS: The PCR-amplified ALR gene was recombin... AIM: To study the protective effect of eukaryotic expression plasmid encoding augmenter of liver regeneration (ALR) on acute hepatic injury and hepatic failure in rats. METHODS: The PCR-amplified ALR gene was recombined with pcDNA3 plasmid, and used to treat rats with acute hepatic injury. The rats with acute hepatic injury induced by intraperitoneal injection of 2 mL/kg 50% carbon tetrachloride (CCl4) were randomly divided into saline control group and recombinant pcDNA3-ALR plasmid treatment groups. Recombinant pcDNA3-ALR plasmid DNA (50 or 200 μg/kg) was injected into the rats with acute hepatic injury intravenously, intraperitoneally, or intravenously and intraperitoneally in combination 4 h after CCl4 administration, respectively. The recombinant plasmid was injected once per 12 h into all treatment groups four times, and the rats were decapitated 12 h after the last injection. Hepatic histopathological alterations were observed after HE staining, the expression of proliferating cell nuclear antigen (PCNA) in liver tissue was detected by immunohistochemical staining, and the level of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) was determined by biochemical method. The recombinant plasmid DNA (200 μg/kg) and saline were intraperitoneally injected into the rats with acute hepatic failure induced by intraperitoneal injection of 4 mL/kg 50% CCl4 after 4 h of CCl4 administration, respectively. Rats living over 96 h were considered as survivals.RESULTS: The sequence of ALR cDNA of recombinant pcDNA3-ALR plasmid was accordant with the reported sequence of rat ALR cDNA. After the rats with acute hepatic injury were treated with recombinant pcDNA3-ALR plasmid, the degree of liver histopathological injury markedly decreased. The pathologic liver tissues, in which hepatic degeneration and necrosis of a small amount of hepatocytes and a large amount of infiltrating inflammatory cells were observed, and they became basically normal in the most effective group after four times of injection of recombinant pcDNA3-ALR plasmid. The indexes of PCNA significantly increased in the recombinant pcDNA3-ALR plasmid treatment groups compared to model group. The level of serum AST and ALT remarkably reduced in recombinant pcDNA3-ALR plasmid treatment groups compared to model group. The results showed that the effect of 200 μg/kg recombinant pcDNA3-ALR plasmid in the rats with acute liver injury was stronger than that of 50μg/kg pcDNA3-ALR DNA.The effect of intravenous injection of recombinant pcDNA3ALR plasmid was better. After the rats with acute hepatic failure were treated with recombinant pcDNA3-ALR plasmid,the survival rate (40%) significantly increased in treatment groups compared to control group (15%, P<0.01).CONCLUSION: The ALR gene may play an important role in relieving acute hepatic injury and hepatic failure by promoting hepatic cell proliferation and reducing level ofAST and ALT in CCl4-intoxicated rats. 展开更多
关键词 真核表达 质体编码 小鼠 动物实验 肝脏重建 急性肝损害 肝功能
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Molecular therapy for hepatic injury and fibrosis:Where are we? 被引量:41
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作者 Colette C Prosser Roy D Yen Jan Wu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第4期509-515,共7页
肝的纤维变性是弯屈的愈合的回答,包含发炎和纤维发生的小径。响应各种各样的侮辱,例如酒精,局部缺血,病毒的代理人,和药或肝毒素, hepatocyte 损坏将在肝由 Kupffer 房间和另外的房间类型引起 cytokines 和另外的可溶的因素的版... 肝的纤维变性是弯屈的愈合的回答,包含发炎和纤维发生的小径。响应各种各样的侮辱,例如酒精,局部缺血,病毒的代理人,和药或肝毒素, hepatocyte 损坏将在肝由 Kupffer 房间和另外的房间类型引起 cytokines 和另外的可溶的因素的版本。这些因素导致肝的星形细胞的激活,它综合大量细胞外的矩阵部件。与长期的损害和纤维变性,肝建筑学和新陈代谢被破坏,最后作为肝硬化和它的复杂并发症表明。除了消除病原学,例如抗病毒的治疗和药理学干预,新奇策略正在被开发直接在细胞的潜水艇和分子的层次探讨肝的损害和纤维变性,这令人鼓舞。与在理解这些机制和小径的改进,在损害给步调音,发信号,激活,和基因表示被分子的形式和分子的其它或基因治疗途径正在指向。这篇文章打算为肝的损害和纤维变性以分子的治疗的当前的地位提供更改并且我们多远从这些新治疗学的形式的临床的利用。 展开更多
关键词 分子治疗 肝损伤 肝纤维化 基因治疗
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Research status of the mechanism and treatment for acute pancreatitis complicated with hepatic injury 被引量:1
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作者 Xiping Zhang Jie Zhang Ping Yang 《Journal of Nanjing Medical University》 2008年第4期199-204,共6页
Acute pancreatitis(AP) is characterized by its sudden onset and rapid progression and is often complicated by liver injury. APinduced liver injury may develop into hepatic failure and even result in death. Thus, it ... Acute pancreatitis(AP) is characterized by its sudden onset and rapid progression and is often complicated by liver injury. APinduced liver injury may develop into hepatic failure and even result in death. Thus, it is of importance to protect liver function and block injury-related pathways. In the pathogenesis of liver injury in AP, inflammatory cytokines, nuclear factor-kappa B(NF- κB) and oxygen free radicals play important roles. The complexity of the mechanism underlying the development of liver injury exerts, to some extent, a contribution to the difficulties in the treatment of this disease. Currently, the drugs used to treat the disease include L-arginine (L-Arg), calcium ion antagonists, somatostatin and a variety of inflammatory mediator inhibitors. Additionally, some traditional Chinese medicines such as tfipterygium, wilfordii, rhubarb and salvia milfiorrhizae may also have some effects. In this article, the pathogenesis of liver injury in AP and its therapy are reviewed. 展开更多
关键词 acute pancreatitis(AP) hepatic injury MECHANISM TREATMENT
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Two clinically relevant pressures of carbon dioxide pneumoperitoneum cause hepatic injury in a rabbit model 被引量:10
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作者 Jun Li Ying-Hai Liu +3 位作者 Zhan-Yong Ye He-Nian Liu Shan Ou Fu-Zhou Tian 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第31期3652-3658,共7页
AIM:To observe the hepatic injury induced by carbon dioxide pneumoperitoneum(CDP) in rabbits,compare the eects olow-and high-pressure pneumoperitoneum,and to determine the degree o hepatic injury induced by these two ... AIM:To observe the hepatic injury induced by carbon dioxide pneumoperitoneum(CDP) in rabbits,compare the eects olow-and high-pressure pneumoperitoneum,and to determine the degree o hepatic injury induced by these two clinically relevant CDP pressures.METHODS:Thirty healthy male New Zealand rabbits weighing 3.0 to 3.5 kg were randomly divided into three groups(n = 10 for each group) and subjected to the ollowing to CDP pressures:no gas control,10 mmHg,or 15 mmHg.Histological changes in liver tissues were observed with hematoxylin and eosin staining and transmission electron microscopy.Liver unction was evaluated using an automatic biochemical analyzer.Adenine nucleotide translocator(ANT) activity in liver tissue was detected with the atractyloside-inhibitor stop technique.Bax and Bcl-2 expression levels were detected bywestern blotting.RESULTS:Liver Functions in the 10 mmHg and 15 mmHg experimental groups were significantly disturbed compared with the control group.After CDP,the levels or alanine transaminase and aspartate transaminase were 77.3 ± 14.5 IU/L and 60.1 ± 11.4 IU/L,respectively,in the 10 mmHg experimental group and 165.1 ± 19.4 IU/L and 103.8 ± 12.3 IU/L,respectively,in the 15 mmHg experimental group,which were all higher than those of the control group(p < 0.05).There was no difference in pre-albumin concentration between the 10 mmHg experimental group and the control group,but the prealbumin level of the 15 mmHg experimental group was significantly lower than that of the control group(p < 0.05).No significant differences were observed in the levels of total bilirubin or albumin among the three groups.After 30 and 60 min of CDP,pH was reduced(p < 0.05) and fa CO2 was elevated(p < 0.05) in the 10 mmHg group compared with controls,and these changes were more pronounced in the 15 mmHg group.Hematoxylin and eosin staining showed no significant change in liver morphology,except for mild hyperemia in the two experimental groups.Transmission electron microscopy showed mild mitochondrial swelling in hepatocytes of the 10 mmHg group,and this was more pronounced in the 15 mmHg group.No significant difference in ANT levels was found between the control and 10 mmHg groups.However,ANT concentration was significantly lower in the 15 mmHg group compared with the control group.The expression of hepatic Bax was significantly increased in the two experimental groups compared with the controls,but there were no differences in Bcl-2 levels among the three groups.Twelve hours after CDP induction,the expression of hepatic Bax was more significant in the 15 mmHg group than in the 10 mmHg group.CONCLUSION:A CDP pressure of 15 mmHg caused more substantial hepatic injury,such as increased levels of acidosis,mitochondrial damage,and apoptosis;therefore,10 mmHg CDP is preferable for laparoscopic operations. 展开更多
关键词 压力诱导 二氧化碳气 肝损伤 临床 家兔 WESTERN印迹 全自动生化分析仪 透射电镜观察
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Kidney response to L-arginine treatment of carbon tetrachloride-induced hepatic injury in mice 被引量:1
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作者 Entsar A. Saad 《Natural Science》 2013年第1期1-6,共6页
Hepatic injury can be induced by the administration of carbon tetrachloride (CCl4) via the production of free radicals. The present work was initiated to investigate the kidney response to hepatic injury induced by CC... Hepatic injury can be induced by the administration of carbon tetrachloride (CCl4) via the production of free radicals. The present work was initiated to investigate the kidney response to hepatic injury induced by CCl4 and its treatment by L-arginine. Female Swiss albino mice were supplied with L-arginine for 6 days (orally, 200 mg/kg body weight) prior or post to hepatic injury induction through i.p. injection with a single dose of CCl4 (20 mg/kg body weight) for 24 h. After hepatic injury induction, renal MDA content was significantly elevated while renal GSH level and the activities of antioxidant enzymes (GR, GPx, GST, catalase, and SOD) were significantly decreased. These results suggest that CCl4 not only induces hepatic injury but also induces kidney dysfunction side by side. Following the treatment with L-arginine, all levels were almost back to normal. Therefore, Larginine administration is found to be an effective protector of both liver and kidney against CCl4-intoxication. 展开更多
关键词 L-ARGININE hepatic injury KIDNEY LIPID PEROXIDATION Antioxidant ENZYMES
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Study on protecting effects of Baicalin and Octreotide on hepatic injury in rats with severe acute pancreatitis 被引量:14
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作者 Xi-Ping Zhang Guang-Hua Feng +7 位作者 Wei Zhu Yang Cai Qi-Jun Yang Tong-Fa Ju Qi xie Wen-Qin Yuan Jie Zhang Zheng Ren 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第42期6551-6559,共9页
AIM: To investigate the protective effects and mechanisms of Baicalin and Octreotide on hepatic injury in rats with severe acute pancreatitis (SAP). METHODS: The SAP rat models were prepared and randomly assigned to t... AIM: To investigate the protective effects and mechanisms of Baicalin and Octreotide on hepatic injury in rats with severe acute pancreatitis (SAP). METHODS: The SAP rat models were prepared and randomly assigned to the model control group, Baicalin treated group, and Octreotide treated group while other healthy rats were assigned to the sham-operated group. Rat mortality, levels of ALT, AST, liver and pancreas pathological changes in all groups were observed at 3, 6 and 12 h after operation. Tissue microarray (TMA) sections of hepatic tissue were prepared to observe expression levels of Bax, Bcl-2 protein and Caspase-3, and changes of apoptotic indexes.RESULTS: Rat survival at 12 h, expression levels of Bax, Caspase-3 protein and apoptotic indexes of liver were all significantly higher in treated groups than in model control group. While the liver and pancreas pathological scores, contents of ALT, AST, and expression levels of Bcl-2 protein were all lower in treated groups than in the model control group. CONCLUSION: Both Baicalin and Octreotide can protect rats with SAP by decreasing the contents of ALT, AST and expression levels of Bcl-2 protein, and improving the expression levels of Bax protein, Caspase-3 protein, and inducing apoptosis. 展开更多
关键词 肝损伤 急性胰腺炎 细胞凋亡 治疗方法
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Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury 被引量:18
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作者 ZHANG Xi-ping WANG Lei ZHANG Jie 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2007年第4期228-236,共9页
Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis(SAP) in mul-tiple organ injury is a hotspot in the surgical field.In clinical practice,the main complicated organ dysf... Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis(SAP) in mul-tiple organ injury is a hotspot in the surgical field.In clinical practice,the main complicated organ dysfunctions are shock,res-piratory failure,renal failure,encephalopathy,with the rate of hepatic diseases being closely next to them.The hepatic injury caused by SAP cannot only aggravate the state of pancreatitis,but also develop into hepatic failure and cause patient death.Its complicated pathogenic mechanism is an obstacle in clinical treatment.Among many pathogenic factors,the changes of vasoac-tive substances,participation of inflammatory mediators as well as OFR(oxygen free radical),endotoxin,etc.may play important roles in its progression. 展开更多
关键词 重症急性胰腺炎 并发症 肝损伤 炎性介质 研究进展
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Pathological and MR-DWI study of the acute hepatic injury model after stem cell transplantation 被引量:6
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作者 Quan-Liang Shang En-Hua Xiao +2 位作者 Qi-Chang Zhou Jian-Guang Luo Hai-Jun Wu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第23期2821-2828,共8页
AIM:To investigate apparent diffusion coefficient (ADC) values as an indication of reconditioning of acute hepatic injury (AHI) after allogeneic mononuclear bone marrow cell (MBMC) transplantation.METHODS:Three groups... AIM:To investigate apparent diffusion coefficient (ADC) values as an indication of reconditioning of acute hepatic injury (AHI) after allogeneic mononuclear bone marrow cell (MBMC) transplantation.METHODS:Three groups were used in our study:a cell transplantation group (n=21),transplantation control group (n=21) and normal control group (n=10).AHI model rabbits in the cell transplantation group were injected with 5 mL of MBMC suspension at multiple sites in the liver and the transplantation controls were injected with 5 mL D-Hanks solution.At the end of the 1st,2nd and 4th wk,7 rabbits were randomly selected from the cell transplantation group and transplantation control group for magnetic resonance diffusion-weighted imaging (MR-DWI) and measurement of the mean ADC values of injured livers.After MR-DWI examination,the rabbits were sacrificed and the livers subjected to pathological examination.Ten healthy rabbits from the normal control group were used for MRDWI examination and measurement of the mean ADC value of normal liver.RESULTS:At all time points,the liver pathological scores from the cell transplantation group were significantly lower than those in the transplantation control group (27.14±1.46 vs 69.29±6.16,22.29±2.29 vs 57.00±1.53,19.00±2.31vs 51.86±6.04,P=0.000).The mean ADC values of the cell transplantation group were significantly higher than the transplantation control group ((1.07±0.07)×10-3 mm2/svs (0.69±0.05)×10-3 mm2/s,(1.41±0.04)×10-3 mm2/s vs (0.84±0.06)×10-3 mm2/s,(1.68±0.04)×10-3 mm2/svs (0.86±0.04)×10-3 mm2/s,P=0.000).The pathological scores of the cell transplantation group and transplantation control group gradually decreased.However,their mean ADC values gradually increased to near that of the normal control.At the end of the 1st wk,the mean ADC values of the cell transplantation group and transplantation control group were significantly lower than those of the normal control group [(1.07±0.07)×10-3 mm2/s vs (1.76±0.03)×10-3 mm2/s,(0.69±0.05)×10-3 mm2/s vs (1.76±0.03)×10-3 mm2/s,P=0.000].At any 2 time points,the pathological scores and the mean ADC values of the cell transplantation group were significantly different (P=0.000).At the end of the 1st wk,the pathological scores and the mean ADC values of the transplantation control group were significantly different from those at the end of the 2nd and 4th wk (P=0.000).However,there was no significant difference between the 2nd and 4th wk (P=0.073 and 0.473,respectively).The coefficient of correlation between the pathological score and the mean ADC value in the cell transplantation group was-0.883 (P=0.000) and-0.762 (P=0.000) in the transplantation control group.CONCLUSION:Tracking the longitudinally dynamic change in the mean ADC value of the AHI liver may reflect hepatic injury reconditioning after allogeneic MBMC transplantation. 展开更多
关键词 干细胞移植 急性肝损伤 病理检查 损伤模型 DWI MR 表观扩散系数 骨髓单个核细胞
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Development of a novel rat model of heterogeneous hepatic injury by injection with colchicine via the splenic vein 被引量:2
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作者 Yan-Yan Zhang Chao-Xu Zhang +6 位作者 Yu Li Xuan Jiang Yong-Fang Wang Yang Sun Jun Wang Wan-Ying Ji Yi Liu 《World Journal of Gastroenterology》 SCIE CAS 2018年第44期5005-5012,共8页
AIM To develop a novel rat model of heterogeneous hepatic injury.METHODS Seventy male Sprague-Dawley rats were randomly divided into a control group(n = 10) and a colchicine group(n =60). A 0.25% colchicine solution(0... AIM To develop a novel rat model of heterogeneous hepatic injury.METHODS Seventy male Sprague-Dawley rats were randomly divided into a control group(n = 10) and a colchicine group(n =60). A 0.25% colchicine solution(0.4 mL/kg) was injected via the splenic vein in the colchicine group to develop a rat model of heterogeneous hepatic injury. An equal volume of normal saline was injected via the splenic vein in the control group. At days 3, 7, and 14 and weeks 4, 8, and 12 after the operation, at least seven rats of the colchicine group were selected randomly for magnetic resonance imaging(MRI) examinations, and then they were euthanized. Ten rats of the control group underwent MRI examinations at the same time points, and then were euthanized at week 12. T2-weighted images(T2 WI) and diffusion weighted imaging(DWI) were used to evaluate the heterogeneous hepatic injury. The heterogeneous injury between the left and right hepatic lobes was assessed on liver sections according to the histological scoring criteria, and correlated with the results of MRI study. RESULTS Obvious pathological changes occurred in the hepatic parenchyma in the colchicine group. Hepatic injury scores were significantly different between the left and right lobes at each time point(P < 0.05). There was a significant difference in apparent diffusion coefficient(ADC) of DWI and liver-to-muscle ratio(LMR) of T2 WI between the left and right lobes of rats in the colchicine group(P < 0.05) at each time point, and similar results were observed between the colchicine and control groups. Besides, there was a significant correlation between hepatic injury scores and ADC values or LMR(r =-0.682, P = 0.000; r =-0.245, P = 0.018).CONCLUSION Injection with colchicine via the splenic vein can be used to successfully develop a rat model of heterogeneous hepatic injury. DWI and T2 WI may help evaluate the heterogeneous injury among liver lobes. 展开更多
关键词 番红花 植物 原料 老鼠 损害 异构 SPRAGUE-DAWLEY 开发
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Roles of Protein Kinase C and Fructose in Hepatic Injury Caused by Obstructive Jaundice
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作者 王剑明 王晖 +1 位作者 肖宝来 邹声泉 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2005年第4期435-438,共4页
Summary: The regulating mechanism in hepatic injury caused by obstructive jaundice (OJ) was examined in this study. Rat hepatocytes were harvested by in situ collagenase perfusion and subjected to primary culture. ... Summary: The regulating mechanism in hepatic injury caused by obstructive jaundice (OJ) was examined in this study. Rat hepatocytes were harvested by in situ collagenase perfusion and subjected to primary culture. The heptocytes were pre-treated with various concentrations of protein kinase C (PKC) agonist PMA and its inhibitor chelerythrine and cultured for 20 min. After the treatment, 50μmol/L glycochenodeoxycholate (GCDC) was added and the cells were cultured for an additional 24 h. Cells were then detected by flow cytometry (FCM) and TUNEL. After hepatocytes were treated with different concentrations of fructose and 100μM GCDC, the cells were examined by FCM and TUNEL. Experimental obstructive jaundice (BDL) was induced by double ligation of the bile duct. After BDL, the rats were fed with or without fructos and sacrificed 3, 7, 14 and 21 days after the ligation. The apoptotic status was observed in liver of all rats with TUNEL and PKC protein in liver of OJ was studied by immunohistochemical method. Our results showed that PMA increased GCDC-induced apoptosis and chelerythrine decreased GCSX-induced apoptosis in a concentration-dependent manner. After the treatment with fructose of different concentrations, 100μM GCDC decreased the apoptotic rate and the apoptotic rate decreased with the increase of fructose concentration. The apoptotic rate of liver was related to the time of OJ. Without the treatment of fructose, PKC and apoptosis index (AI) were highest 14 days after the bile duct ligation. With the treatment of fructose, apoptosis index (AI) and PKC were decreased from the 14th day after the bile duct ligation. It is concluded that PKC is involved in the regulation of apoptosis in the liver cells with OJ and plays important roles in the development and progression of liver injury caused by OJ. Fructose can protect hepatocytes in the bile salt-induced apoptosis by regulating PKC. 展开更多
关键词 CHOLESTASIS hepatic injury protein kinase C FRUCTOSE
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