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基于均匀设计的祛湿化瘀复方抗脂毒性作用的主效应中药分析 被引量:15
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作者 陈少东 胡义扬 +5 位作者 冯琴 李红山 李雪梅 许丽莉 鲜洁晨 张宁 《中国中西医结合杂志》 CAS CSCD 北大核心 2008年第5期421-425,共5页
目的观察祛湿化瘀复方的主效应中药或不同组合对游离脂肪酸(free fatty acid,FFA)诱导人肝癌细胞株(HepG2)细胞脂肪沉积和肿瘤坏死因子α(turmor necrosis factor α,TNF-α)分泌的作用,探索中药复方药理作用相应物质基础的分析方法。... 目的观察祛湿化瘀复方的主效应中药或不同组合对游离脂肪酸(free fatty acid,FFA)诱导人肝癌细胞株(HepG2)细胞脂肪沉积和肿瘤坏死因子α(turmor necrosis factor α,TNF-α)分泌的作用,探索中药复方药理作用相应物质基础的分析方法。方法采用FFA诱导HepG2细胞脂肪沉积和TNF-α分泌的体外细胞模型和药物血清技术,运用数学模型"均匀设计法",根据复方中的5味中药(茵陈、栀子、虎杖、田基黄、姜黄),选用U11(1110)表进行组方设计所得10种中药组合进行干预,以对甘油三酯(triglyceride,TG)及TNF-α的抑制效应作为考察指标,筛选主效应中药或组合,并重新区间分组验证。结果茵陈和田基黄在高剂量组合时有显著降低细胞TG及TNF-α含量的效应,与全方比较差异无统计学意义,其中单用茵陈也可显著降低细胞TG及TNF-α含量。结论茵陈及其与田基黄的组合是祛湿化瘀复方抑制FFA诱导HepG2细胞脂肪沉积和TNF-α分泌作用的主效应中药;应用均匀设计与药效学分析的方法可有效分析中药复方针对某一作用环节的主效应中药或组合。 展开更多
关键词 祛湿化瘀复方 肝脂毒性 游离肪酸 均匀设计
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肝再生增强因子调控线粒体功能稳态在棕榈酸诱导肝细胞脂毒性细胞模型中的作用
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作者 周光 施晓雷 《南京医科大学学报(自然科学版)》 CAS CSCD 北大核心 2019年第10期1421-1425,共5页
目的:研究肝细胞脂毒性细胞模型中线粒体内肝再生增强因子(augmenter of liver regeneration,ALR)与线粒体功能障碍之间的关系。方法:以无脂肪酸的10%牛血清蛋白(bull serum albumin,BSA)处理L-O2细胞为对照(BSA组),0.2 mmol/L棕榈酸(pa... 目的:研究肝细胞脂毒性细胞模型中线粒体内肝再生增强因子(augmenter of liver regeneration,ALR)与线粒体功能障碍之间的关系。方法:以无脂肪酸的10%牛血清蛋白(bull serum albumin,BSA)处理L-O2细胞为对照(BSA组),0.2 mmol/L棕榈酸(palmitic acid,PA)处理L-O2细胞为脂毒性细胞模型(PA组),并在构建ALR过表达(ALR-OE组)及对照(Vector组)细胞后,分别接受BSA和PA处理,CCK-8法检测细胞活力、乳酸脱氢酶(lactic dehydrogenase,LDH)检测试剂盒检测脂毒性、JC-1染色分析线粒体膜电位、流式凋亡检测分析细胞凋亡,Western bolt检测ALR、Bax、Bcl-2、细胞色素C等蛋白表达水平。结果:与BSA组相比,PA组细胞内脂滴增多、细胞活力下降50%、LDH释放增加13倍,线粒体内ALR表达则明显降低。BSA处理下Vector组和ALR-OE组无明显差异,而PA刺激后ALR-OE组相较于Vector组,细胞活力增加约16%,LDH释放减少约40%,线粒体膜电位增加约18%,细胞色素C释放减少,细胞凋亡减少。结论:ALR参与肝细胞脂毒性的发生,靶向调控ALR可在一定程度上抑制脂毒性的发生。 展开更多
关键词 线粒体 细胞毒性细胞模型 再生增强因子
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肝脂消胶囊治疗肝炎合并脂肪肝52例 被引量:1
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作者 隋继成 孙志云 《光明中医》 2007年第1期87-88,共2页
本文通过肝脂消胶囊治疗肝炎合并脂肪肝52例的统计显示:本品治疗后实验室指标改善较明显,与治疗前相比有显著差异(P值:SB<0·05,其他几项均<0·01)。
关键词 消胶囊/病毒性
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祛湿化瘀方对游离脂肪酸诱导的HepG2细胞脂肪沉积和TNF-α分泌的抑制作用 被引量:18
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作者 张慧 胡义扬 +4 位作者 冯琴 陈少东 许丽莉 成扬 张宁 《中国中西医结合杂志》 CAS CSCD 北大核心 2007年第12期1105-1109,共5页
目的研究祛湿化瘀方对体外肝脂毒性模型脂肪沉积和肿瘤坏死因子α(tumor necrosis factorα,TNF-α)分泌的影响,以进一步探究该方防治脂肪肝的作用机理方法复制游离脂肪酸(free fatty acid,FFA)诱导的HepG2细胞脂肪变性和TNF-α分泌脂... 目的研究祛湿化瘀方对体外肝脂毒性模型脂肪沉积和肿瘤坏死因子α(tumor necrosis factorα,TNF-α)分泌的影响,以进一步探究该方防治脂肪肝的作用机理方法复制游离脂肪酸(free fatty acid,FFA)诱导的HepG2细胞脂肪变性和TNF-α分泌脂毒性模型。设正常组、模型组和不同浓度药物血清组。分别观察上清中TNF-α含量,细胞内甘油三酯(triglyceride,TG)含量,细胞油红染色和电镜超微结构变化,细胞TNF-α蛋白表达及其基因表达。结果FFA刺激24 h后,模型组细胞内脂肪沉积明显,其TG含量显著高于正常组(P<0.01),同时上清中TNF-α含量、细胞内TNF-α的蛋白表达及其mRNA表达显著增强。而10%药物血清组细胞内TG含量及上清中TNF-α含量显著低于模型组(均P<0.01),其脂肪沉积、细胞内TNF-α的蛋白表达及其mRNA表达也明显轻于模型组。 展开更多
关键词 祛湿化瘀方 肝脂毒性 游离肪酸 甘油三酯 肿瘤坏死因子-α
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茵陈醇提物抗游离脂肪酸对体外培养HepG2细胞脂毒性的作用及机制研究 被引量:15
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作者 陈少东 冯琴 +4 位作者 彭景华 许丽莉 刘平 刘成 胡义扬 《中国中药杂志》 CAS CSCD 北大核心 2009年第18期2373-2378,共6页
目的:研究茵陈醇提物对游离脂肪酸刺激HepG2细胞所致肝脂毒性的抑制作用及机制。方法:制备大鼠的正常血清和药物血清,在经毒性试验确定无药物毒性的前提下,分设正常组、模型组和茵陈醇提物组(10%,1%,0.1%3个剂量),以相应浓度的正常血清... 目的:研究茵陈醇提物对游离脂肪酸刺激HepG2细胞所致肝脂毒性的抑制作用及机制。方法:制备大鼠的正常血清和药物血清,在经毒性试验确定无药物毒性的前提下,分设正常组、模型组和茵陈醇提物组(10%,1%,0.1%3个剂量),以相应浓度的正常血清和药物血清培养HepG2细胞,同时添加长链游离脂肪酸(FFA)刺激HepG2细胞24 h。观察:①细胞上清肿瘤坏死因子(TNF-α)含量(ELISA法);②细胞内甘油三酯(TG)含量、细胞脂肪油红O染色;③细胞内磷酸化κB抑制蛋白(P-IκB)、组织蛋白酶B(ctsb)、凋亡抑制基因相关X蛋白(Bax)蛋白表达(W estern B lotting法);④细胞TNF-,αctsb和Bax基因表达(real-tim e PCR);⑤细胞内ctsb的表达和分布(免疫荧光法)。结果:模型组细胞内TG及上清TNF-α含量显著升高,分别达(590±186)mg.g-1,(77±11)pg.mg-1,细胞内ctsb,P-IκB的蛋白表达以及ctsb,TNF-α的mRNA表达显著增强;而10%茵陈醇提物组细胞内TG和上清TNF-α含量较模型组显著降低,仅为(335±54)mg.g-1,(55±7)pg.mg-1,且显著抑制细胞内ctsb,P-IκB的蛋白表达以及ctsb,TNF-α的mRNA表达。结论:茵陈醇提物对FFA诱导的HepG2细胞脂肪变性,TNF-α分泌有显著的抑制作用,其作用与抑制ctsb等基因和蛋白表达有关。 展开更多
关键词 茵陈醇提物 游离肪酸 HEPG2细胞 肝脂毒性
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茵陈蒿汤抗游离脂肪酸对HepG2细胞脂毒性作用的效应中药研究 被引量:10
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作者 陈少东 周海虹 +3 位作者 李雪梅 林锦培 范应 徐维佳 《中华中医药杂志》 CAS CSCD 北大核心 2010年第9期1381-1384,共4页
目的:探讨对游离脂肪酸(FFA)诱导人肝癌细胞株(HepG2)细胞脂肪沉积和对肿瘤坏死因子(TNF-α)分泌有显著抑制作用的茵陈蒿汤的效应中药或组合。方法:采用FFA诱导HepG2细胞脂肪沉积和TNF-α分泌的体外细胞模型和药物血清技术,运用数学模型... 目的:探讨对游离脂肪酸(FFA)诱导人肝癌细胞株(HepG2)细胞脂肪沉积和对肿瘤坏死因子(TNF-α)分泌有显著抑制作用的茵陈蒿汤的效应中药或组合。方法:采用FFA诱导HepG2细胞脂肪沉积和TNF-α分泌的体外细胞模型和药物血清技术,运用数学模型"均匀设计法",根据复方中的3味中药(茵陈、栀子、大黄),选用U7(76)表进行组方设计所得6种中药组合进行干预,以对甘油三酯(TG)及TNF-α的抑制效应作为考察指标,筛选效应中药或组合,并重新区间分组验证。结果:茵陈和栀子在高剂量组合时有显著降低细胞TG及TNF-α含量的效应,与全方无显著性差异,其中单一茵陈也可显著降低细胞TG及TNF-α含量。结论:茵陈及其与栀子的组合是茵陈蒿汤抑制FFA诱导HepG2细胞脂肪沉积和TNF-α分泌作用的效应中药。 展开更多
关键词 茵陈蒿汤 HEPG2细胞 肝脂毒性 游离肪酸 甘油三酯 肿瘤坏死因子Α 均匀设计
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Pathophysiology of insulin resistance and steatosis in patients with chronic viral hepatitis 被引量:8
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作者 Metin Basaranoglu Gkcen Basaranoglu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第36期4055-4062,共8页
Chronic hepatitis due to any cause leads to cirrhosis and end-stage liver disease.A growing body of literature has also shown that fatty liver due to overweight or obesity is a leading cause of cirrhosis.Due to the ob... Chronic hepatitis due to any cause leads to cirrhosis and end-stage liver disease.A growing body of literature has also shown that fatty liver due to overweight or obesity is a leading cause of cirrhosis.Due to the obesity epidemic,fatty liver is now a significant problem in clinical practice.Steatosis has an impact on the acceleration of liver damage in patients with chronic hepatitis due to other causes.An association between hepatitis C virus (HCV) infection,steatosis and the onset of insulin resistance has been reported.Insulin resistance is one of the leading factors for severe fibrosis in chronic HCV infections.Moreover,hyperinsulinemia has a deleterious effect on the management of chronic HCV.Response to therapy is increased by decreasing insulin resistance by weight loss or the use of thiazolidenediones or metformin.The underlying mechanisms of this complex interaction are not fully understood.A direct cytopathic effect of HCV has been suggested.The genomic structure of HCV (suggesting that some viral sequences are involved in the intracellular accumulation of triglycerides),lipid metabolism,the molecular links between the HCV core protein and lipid droplets (the core protein of HCV and its transcriptional regulatory function which induce a triglyceride accumulation in hepatocytes) and increased neolipogenesis and inhibited fatty acid degradation in mitochondria have been investigated. 展开更多
关键词 ADIPOCYTOKINES Fatty acids Hepatitis B virus Hepatitis C virus Inducible nitric oxide synthase Insulin resistance Signal transduction and activator of transcription-3 STEATOSIS Sterol regulatory elementbinding protein-1c Suppressors of cytokine signaling Tumor necrosis factor-α
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Mechanisms and significance of liver steatosis in hepatitis C virus infection 被引量:16
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作者 francesco Negro 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第42期6756-6765,共10页
The pathogenesis of liver damage associated with chronic hepatitis C virus (HCV) infection is thought to be largely immunomediated. However, some frequent histoo pathological features, such as steatosis, suggest a d... The pathogenesis of liver damage associated with chronic hepatitis C virus (HCV) infection is thought to be largely immunomediated. However, some frequent histoo pathological features, such as steatosis, suggest a direct cytopathic effect of HCV. The direct responsibility of HCV in the pathogenesis of steatosis is shown by: (1) the association with HCV genotype 3 infection, suggesting that some viral sequences are involved in the intracellular aco cumulation of lipids; (2) the correlation between severity of steatosis and HCV replication levels; (3) association between response to treatment and disappearance of steatosis. Experimental studies have shown that the nuo cleocapsid protein of HCV (core protein) is capable and sufficient to induce lipid accumulation in hepatocytes. Moreover, the observation that chronic hepatitis C pao tients have reduced serum levels of ApoB suggests an interference with the very-low density lipoprotein (VLDL) assembly, although other mechanisms are possible. In patients with sustained virological response induced by antiviral therapy, such levels are normalized. Other obo servations suggest that the pathogenesis of steatosis in chronic hepatitis C is not solely due to HCV. The origin of the mild steatosis observed in most patients may be metabolic, since its severity correlates with body mass index and insulin resistance. Most studies have shown a correlation between presence and/or severity of steatosis and fibrosis stage, but it is unclear whether this effect is direct or mediated by the associated insulin resistance, increased susceptibility to apoptosis, or by inflammao tory cytokines. Finally, steatosis negatively influences the rate of response to antiviral treatment, as confirmed by large clinical trials. Management of steatosis in chronic hepatitis C requires knowledge of its pathogenesis and may involve both life-style changes and pharmacological interventions, although the latter remain largely experio mental. 展开更多
关键词 Hepatitis C FIBROSIS Insulin Resistance Insulin signaling
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Innate immune reactivity of the liver in rats fed a choline-deficient L-amino-acid-defined diet 被引量:5
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作者 Hideto Kawaratani Tatsuhiro Tsujimoto +4 位作者 Toshiyuki Kitazawa Mitsuteru Kitade Hitoshi Yoshiji Masahito Uemura Hiroshi Fukui 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第43期6655-6661,共7页
AIM: To investigate the innate immune reactivity of tumor necrosis factor-alpha (TNF-α), Toll-like receptor 4 (TLR4), and CD14 in the liver of non-alcoholic steatohepatitis (NASH) model rats. METHODS: Male F3... AIM: To investigate the innate immune reactivity of tumor necrosis factor-alpha (TNF-α), Toll-like receptor 4 (TLR4), and CD14 in the liver of non-alcoholic steatohepatitis (NASH) model rats. METHODS: Male F344 rats were fed a cholinedeficient L-amino-acid-defined (CDAA) diet. The rats were killed after 4 or 8 wk of the diet, and their livers were removed for immunohistochemical investigation and RNA extraction. The liver specimens were immunostained for TNF-α, TLR4, and CD14. The gene expressions of TNF-α, TLR4, and CD14 were determined by reverse-transcriptase polymerase chain reaction (RT-PCR). Kupffer cells were isolated from the liver by Percoll gradient centrifugation, and were then cultured to measure TNF-α production. RESULTS: The serum and liver levels of TNF-~ in the CDAA-fed rats increased significantly as compared with the control group, as did the immunohistochemical values and gene expressions of TNF-α, TLR4, and CD14 with the progression of steatohepatitis. TNF-α production from the isolated Kupffer cells of the CDAAfed rats was elevated by lipopolysaccharide stimulation. CONCLUSION: The expressions of TNF-α, TLR4, and CD14 increased in the NASH model, suggesting that 展开更多
关键词 Nonalcoholic steatohepatitis Kupffer cells Toll-like receptor 4 CD14 ENDOTOXINS Tumor necrosisfactor-alpha
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Guillain-Barrésyndrome following hepatitis E 被引量:1
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作者 Jean Philippe Loly Estelle Rikir +5 位作者 Maxime Seivert Emile Legros Pierre Defrance Jacques Belaiche Gustave Moonen Jean Delwaide 《World Journal of Gastroenterology》 SCIE CAS CSCD 2009年第13期1645-1647,共3页
Guillain-Barrésyndrome(GBS)is often triggered by a preceding bacterial or viral infection.Occasionally,it has been observed in association with acute hepatitis A,B and C,and three cases have been previously descr... Guillain-Barrésyndrome(GBS)is often triggered by a preceding bacterial or viral infection.Occasionally,it has been observed in association with acute hepatitis A,B and C,and three cases have been previously described in India in which GBS was associated with acute hepatitis E.A molecular mimicry mechanism is supposed to be involved in the pathogenesis of GBS triggered by infectious agents,although the nature of the shared epitopes has not been characterized in most instances,including that in the case of hepatotropic viruses.We report a case of GBS following acute hepatitis E in a European individual.The presence of antiganglioside GM2 antibodies in this patient suggested molecular mimicry involving ganglioside GM2 in the pathogenesis of GBS associated with hepatitis E. 展开更多
关键词 GANGLIOSIDES Guillain-Barré syndrome Hepatitis E Molecular mimicry Viral hepatitis
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Ion Channels as Antivirus Targets
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作者 Xin LIANG Zhi-yuan LI 《Virologica Sinica》 SCIE CAS CSCD 2010年第4期267-280,共14页
Ion channels are membrane proteins that are found in a number of viruses and which are of crucial physiological importance in the viral life cycle. They have one common feature in that their action mode involves a cha... Ion channels are membrane proteins that are found in a number of viruses and which are of crucial physiological importance in the viral life cycle. They have one common feature in that their action mode involves a change of electrochemical or proton gradient across the bilayer lipid membrane which modulates viral or cellular activity. We will discuss a group of viral channel proteins that belong to the viroproin family, and which participate in a number of viral functions including promoting the release of viral particles from cells. Blocking these channel-forming proteins may be "lethal", which can be a suitable and potential therapeutic strategy. In this review we discuss seven ion channels of viruses which can lead serious infections in human beings: M2 of influenza A, NB and BM2 of influenza B, CM2 of influenza C, Vpu of HIV-1, p7 of HCV and 2B of picomaviruses. 展开更多
关键词 Viral ion channel Antiviral therapy Viruses AMANTADINE
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Potential chronic liver toxicity in rats orally administered an ethanol extract of Huangqin(Radix Scutellariae Baicalensis) 被引量:2
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作者 Yi Yan Zhao Yong +6 位作者 Li Chunying Zhang Yushi Bin Yang Yuan Yalan Pan Chen Wang Lianmei Liang Aihua 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2018年第2期242-256,共15页
OBJECTIVE: To investigate the potential chronic liver toxicity of oral administration of ethanol extract of Huangqin(Radix Scutellariae Baicalensis)(SBE) in Wistar rats.METHODS: SBE was administered to rats by gavage ... OBJECTIVE: To investigate the potential chronic liver toxicity of oral administration of ethanol extract of Huangqin(Radix Scutellariae Baicalensis)(SBE) in Wistar rats.METHODS: SBE was administered to rats by gavage for 26 weeks, at doses of 300, 1250, or 2500 mg·kg-1·d-1 respectively. The rats were euthanized at the end of 13 and 26 weeks daily oral dosing and following 4 weeks of recovery time. The changes of hematology, urinary, blood biochemistry and histomorphology were examined at each time point and focus on liver function and histological changes.RESULTS: When SBE at a dose of up to 2500 mgkg-1 d-1 was fed to male and female rats for 2··6 weeks, the liver tissue showed some inflammatory change that predominated by leukocyte infiltrationbut returned to normal after withdrawal. In addition, high-dose SBE treatment of 26 weeks in rats,glucose, electrolyte and lipid levels also have some changes. In addition, there are no other functional or organic lesions related to SBE treatment.CONCLUSIONS: Long-term and high-dose SBE may cause liver damage, however, the structural damage of the liver can be restored after the ethanol extract stopping. SBE will be well-tolerated for long-term use as a drug or health food, but in order to ensure drug safety, liver function, and serum glucose, electrolyte and lipid levels should be monitored when using SBE long term. 展开更多
关键词 Scutellaria baicalensis Toxicity tests CHRONIC LIVER ADMINISTRATION ORAL
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