期刊文献+
共找到295篇文章
< 1 2 15 >
每页显示 20 50 100
Impact of interleukin 6 levels on acute lung injury risk and disease severity in critically ill sepsis patients 被引量:2
1
作者 Ya Liu Li Chen 《World Journal of Clinical Cases》 SCIE 2024年第23期5374-5381,共8页
BACKGROUND Sepsis is a life-threatening condition characterized by a dysregulation of the host response to infection that can lead to acute lung injury(ALI)and multiple organ dysfunction syndrome(MODS).Interleukin 6(I... BACKGROUND Sepsis is a life-threatening condition characterized by a dysregulation of the host response to infection that can lead to acute lung injury(ALI)and multiple organ dysfunction syndrome(MODS).Interleukin 6(IL-6)is a pro-inflammatory cytokine that plays a crucial role in the pathogenesis of sepsis and its complications.AIM To investigate the relationship among plasma IL-6 levels,risk of ALI,and disease severity in critically ill patients with sepsis.METHODS This prospective and observational study was conducted in the intensive care unit of a tertiary care hospital between January 2021 and December 2022.A total of 83 septic patients were enrolled.Plasma IL-6 levels were measured upon admission using an enzyme-linked immunosorbent assay.The development of ALI and MODS was monitored during hospitalization.Disease severity was evaluated by Acute Physiology and Chronic Health Evaluation II(APACHE II)and Sequential Organ Failure Assessment(SOFA)scores.RESULTS Among the 83 patients with sepsis,38(45.8%)developed ALI and 29(34.9%)developed MODS.Plasma IL-6 levels were significantly higher in patients who developed ALI than in those without ALI(median:125.6 pg/mL vs 48.3 pg/mL;P<0.001).Similarly,patients with MODS had higher IL-6 levels than those without MODS(median:142.9 pg/mL vs 58.7 pg/mL;P<0.001).Plasma IL-6 levels were strongly and positively correlated with APACHE II(r=0.72;P<0.001)and SOFA scores(r=0.68;P<0.001).CONCLUSIONElevated plasma IL-6 levels in critically ill patients with sepsis were associated with an increased risk of ALI andMODS.Higher IL-6 levels were correlated with greater disease severity,as reflected by higher APACHE II andSOFA scores.These findings suggest that IL-6 may serve as a biomarker for predicting the development of ALI anddisease severity in patients with sepsis. 展开更多
关键词 SEPSIS Acute lung injury Multiple organ dysfunction syndrome INTERLEUKIN-6 BIOMARKER Disease severity
下载PDF
MicroRNA-451 from Human Umbilical Cord-Derived Mesenchymal Stem Cell Exosomes Inhibits Alveolar Macrophage Autophagy via Tuberous Sclerosis Complex 1/Mammalian Target of Rapamycin Pathway to Attenuate Burn-Induced Acute Lung Injury in Rats 被引量:1
2
作者 Zhigang Jia Lin Li +5 位作者 Peng Zhao Guo Fei Shuangru Li Qinqin Song Guangpeng Liu Jisong Liu 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2024年第9期1030-1043,共14页
Objective Our previous studies established that microRNA(miR)-451 from human umbilical cord mesenchymal stem cell-derived exosomes(hUC-MSC-Exos)alleviates acute lung injury(ALI).This study aims to elucidate the mechan... Objective Our previous studies established that microRNA(miR)-451 from human umbilical cord mesenchymal stem cell-derived exosomes(hUC-MSC-Exos)alleviates acute lung injury(ALI).This study aims to elucidate the mechanisms by which miR-451 in hUC-MSC-Exos reduces ALI by modulating macrophage autophagy.Methods Exosomes were isolated from hUC-MSCs.Severe burn-induced ALI rat models were treated with hUC-MSC-Exos carrying the miR-451 inhibitor.Hematoxylin-eosin staining evaluated inflammatory injury.Enzyme-linked immunosorbnent assay measured lipopolysaccharide(LPS),tumor necrosis factor-α,and interleukin-1βlevels.qRT-PCR detected miR-451 and tuberous sclerosis complex 1(TSC1)expressions.The regulatory role of miR-451 on TSC1 was determined using a dual-luciferase reporter system.Western blotting determined TSC1 and proteins related to the mammalian target of rapamycin(mTOR)pathway and autophagy.Immunofluorescence analysis was conducted to examine exosomes phagocytosis in alveolar macrophages and autophagy level.Results hUC-MSC-Exos with miR-451 inhibitor reduced burn-induced ALI and promoted macrophage autophagy.MiR-451 could be transferred from hUC-MSCs to alveolar macrophages via exosomes and directly targeted TSC1.Inhibiting miR-451 in hUC-MSC-Exos elevated TSC1 expression and inactivated the mTOR pathway in alveolar macrophages.Silencing TSC1 activated mTOR signaling and inhibited autophagy,while TSC1 knockdown reversed the autophagy from the miR-451 inhibitor-induced.Conclusion miR-451 from hUC-MSC exosomes improves ALI by suppressing alveolar macrophage autophagy through modulation of the TSC1/mTOR pathway,providing a potential therapeutic strategy for ALI. 展开更多
关键词 Acute lung injury Human umbilical cord mesenchymal stem cell-derived exosomes MicroRNA-451 Tuberous sclerosis complex 1 Mammalian target of rapamycin pathway AUTOPHAGY
下载PDF
Mogroside IIE,an in vivo metabolite of sweet agent,alleviates acute lung injury via Pla2g2a-EGFR inhibition
3
作者 Weichao Lü Guoqing Ren +2 位作者 Kuniyoshi Shimizu Renshi Li Chaofeng Zhang 《Food Science and Human Wellness》 SCIE CSCD 2024年第1期299-312,共14页
In the face of increasingly serious environmental pollution,the health of human lung tissues is also facing serious threats.Mogroside IIE(M2E)is the main metabolite of sweetening agents mogrosides from the anti-tussiv... In the face of increasingly serious environmental pollution,the health of human lung tissues is also facing serious threats.Mogroside IIE(M2E)is the main metabolite of sweetening agents mogrosides from the anti-tussive Chinese herbal Siraitia grosvenori.The study elucidated the anti-inflammatory action and molecular mechanism of M2E against acute lung injury(ALI).A lipopolysaccharide(LPS)-induced ALI model was established in mice and MH-S cells were employed to explore the protective mechanism of M2E through the western blotting,co-immunoprecipitation,and quantitative real time-PCR analysis.The results indicated that M2E alleviated LPS-induced lung injury through restraining the activation of secreted phospholipase A2 type IIA(Pla2g2a)-epidermal growth factor receptor(EGFR).The interaction of Pla2g2a and EGFR was identified by co-immunoprecipitation.In addition,M2E protected ALI induced with LPS against inflammatory and damage which were significantly dependent upon the downregulation of AKT and m TOR via the inhibition of Pla2g2a-EGFR.Pla2g2a may represent a potential target for M2E in the improvement of LPS-induced lung injury,which may represent a promising strategy to treat ALI. 展开更多
关键词 Mogroside IIE Acute lung injury Secreted phospholipase A2 type IIA(Pla2g2a) Epidermal growth factor receptor(EGFR)
下载PDF
Research Progress on the Pathogenesis of Acute Lung Injury(ALI)
4
作者 Jincun LI Wenyu MA Gang LI 《Medicinal Plant》 2024年第4期122-128,共7页
In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excess... In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excessive oxidative stress,cell death,endoplasmic reticulum stress,coagulation dysfunction,and weakened aquaporin function. 展开更多
关键词 Acute lung injury(ALI) Pathogenesis Inflammatory responses Oxidative stress Cell death Endoplasmic reticulum stress COAGULOPATHY Downregulation of aquaporin
下载PDF
Mechanisms and Research Progress of Traditional Chinese Medicine Regulating NF-κB in the Treatment of Acute Lung Injury/Acute Respiratory Distress Syndrome
5
作者 Wanzhao Zuo Fanian Tian +3 位作者 Jia Ke Cheng Jiang Yi Yang Cong He 《Chinese Medicine and Natural Products》 CAS 2024年第3期93-105,共13页
Acute lung injury(ALI)has multiple causes and can easily progress to acute respiratory distress syndrome(ARDS)if not properly treated.Nuclear factorκB(NF-κB)is a key pathway in the treatment of ALI/ARDS.By exploring... Acute lung injury(ALI)has multiple causes and can easily progress to acute respiratory distress syndrome(ARDS)if not properly treated.Nuclear factorκB(NF-κB)is a key pathway in the treatment of ALI/ARDS.By exploring the relevance of NF-κB and the pathogenesis of this disease,it was found that this disease was mainly associated with inflammation,dysfunction of the endothelial barrier,oxidative stress,impaired clearance of alveolar fluid,and coagulation disorders.Traditional Chinese medicine(TCM)has the characteristics of multitargeting,multipathway effects,and high safety,which can directly or indirectly affect the treatment of ALI/ARDS.This article summarizes the mechanism and treatment strategies of TCM in recent years through intervention in the NF-κB-related signaling pathways for treating ALI/ARDS.It provides an overview from the perspectives of Chinese herbal monomers,TCM couplet medicines,TCM injections,Chinese herbal compounds,and Chinese herbal preparations,offering insights into the prevention and treatment of ALI/ARDS with TCM. 展开更多
关键词 acute lung injury acute respiratory distress syndrome traditional Chinese medicine NF-ΚB
下载PDF
Research Progress on the Prevention of Premature Infant Lung Injury and Neonatal Respiratory Support
6
作者 Jianghe Yu Simin Cai 《Expert Review of Chinese Medical》 2024年第1期18-21,共4页
In the past 40 years,advances in neonatal intensive care unit(NICU)technology have enabled premature infants with lower birth weight and younger gestational age to survive.But with it comes an increase in the incidenc... In the past 40 years,advances in neonatal intensive care unit(NICU)technology have enabled premature infants with lower birth weight and younger gestational age to survive.But with it comes an increase in the incidence of long-term respiratory dysfunction,mainly in the form of bronchopulmonary dysplasia(BPD).Preventing lung injury is crucial for preventing BPD and improving the long-term prognosis of premature infants.Therefore,how to avoid ventilator-associated lung injury has become a focus of clinical and scientific research in premature infants in recent years.This article will elaborate on the susceptibility and pathophysiology of premature infant lung injury,ventilation strategies for preventing lung injury,and new advances in neonatal respiratory support. 展开更多
关键词 premature infants lung injury respiratory support research progress
下载PDF
Modulating the crosstalk between macrophage and Th17: potential mechanism of natural products on acute lung injury
7
作者 Xi-Xing Fang Han-Zhou Li +7 位作者 Ning Wang Wen-Ju He Yu-Lin Wu Li-Ying Guo Li-Wei Xing Wei-Bo Wen Qian-Qian Wan Huan-Tian Cui 《Biomedical Engineering Communications》 2024年第3期31-37,共7页
Sepsis is a life-threatening multiple organ dysfunction syndrome caused by the imbalance of the immune response to infection,featuring complex and variable conditions,and is one of the leading causes of mortality in I... Sepsis is a life-threatening multiple organ dysfunction syndrome caused by the imbalance of the immune response to infection,featuring complex and variable conditions,and is one of the leading causes of mortality in ICU patients.Lung injury is a common organ damage observed in sepsis patients.Macrophages and Th17 cells,as crucial components of innate and adaptive immunity,play pivotal roles in the development of sepsis-induced acute lung injury(ALI).This review summarizes the alterations and mechanisms of macrophages and Th17 cells in sepsis-induced ALI.By focusing on the“cross-talk”between macrophages and Th17 cells,this review aims to provide a solid theoretical foundation for further exploring the therapeutic targets of traditional Chinese medicine formulas in the treatment of sepsis complicated with ALI,thereby offering insights and guidance for the clinical application of traditional Chinese medicine in managing sepsis-associated ALI. 展开更多
关键词 sepsis-induced acute lung injury MACROPHAGES Th17 cells traditional Chinese medicine
下载PDF
Acute lung injury and ARDS in acute pancreatitis: Mechanisms and potential intervention 被引量:66
8
作者 Roland Andersson 《World Journal of Gastroenterology》 SCIE CAS CSCD 2010年第17期2094-2099,共6页
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in acute pancreatitis still represents a substantial problem,with a mortality rate in the range of 30%-40%.The present review evaluates underlying... Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in acute pancreatitis still represents a substantial problem,with a mortality rate in the range of 30%-40%.The present review evaluates underlying pathophysiological mechanisms in both ALI and ARDS and potential clinical implications.Several mediators and pathophysiological pathways are involved during the different phases of ALI and ARDS.The initial exudative phase is characterized by diffuse alveolar damage,microvascular injury and influx of inflammatory cells.This phase is followed by a fibro-proliferative phase with lung repair,type Ⅱ pneumocyte hypoplasia and proliferation of fibroblasts.Proteases derived from polymorphonuclear neutrophils,various pro-inflammatory mediators,and phospholipases are all involved,among others.Contributing factors that promote pancreatitis-associated ALI may be found in the gut and mesenteric lymphatics.There is a lack of complete understanding of the underlying mechanisms,and by improving our knowledge,novel tools for prevention and intervention may be developed,thus contributing to improved outcome. 展开更多
关键词 Acute lung injury Acute respiratory distress syndrome Acute pancreatitis ETIOLOGY PATHOPHYSIOLOGY
下载PDF
Review:Acute lung injury/acute respiratory distress syndrome (ALI/ARDS): the mechanism,present strategies and future perspectives of therapies 被引量:55
9
作者 LUH Shi-ping CHIANG Chi-huei 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2007年第1期60-69,共10页
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS), which manifests as non-cardiogcnic pulmonary edema, respiratory distress and hypoxemia, could be resulted from various processes that directly or ind... Acute lung injury/acute respiratory distress syndrome (ALI/ARDS), which manifests as non-cardiogcnic pulmonary edema, respiratory distress and hypoxemia, could be resulted from various processes that directly or indirectly injure the lung. Extensive investigations in experimental models and humans with ALI/ARDS have revealed many molecular mechanisms that offer therapeutic opportunities for cell or gene therapy. Herein the present strategies and future perspectives of the treatment for ALI/ARDS, include the ventilatory, pharmacological, as well as cell therapies. 展开更多
关键词 Acute lung injury Acute respiratory distress syndrome VENTILATOR Cell therapy
下载PDF
Leptin treatment ameliorates acute lung injury in rats with cerulein-induced acute pancreatitis 被引量:24
10
作者 Fatma Ayca Gultekin Mustafa Kerem +3 位作者 Ertan Tatlicioglu Aysel Aricioglu Cigdem Unsal Neslihan Bukan 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第21期2932-2938,共7页
AIM:To determine the effect of exogenous leptin on acute lung injury (ALI) in cerulein-induced acute pancreatitis (AP). METHODS:Forty-eight rats were randomly divided into 3 groups. AP was induced by intraperitoneal (... AIM:To determine the effect of exogenous leptin on acute lung injury (ALI) in cerulein-induced acute pancreatitis (AP). METHODS:Forty-eight rats were randomly divided into 3 groups. AP was induced by intraperitoneal (i.p.) injection of cerulein (50 μg/kg) four times,at 1 h intervals. The rats received a single i.p. injection of 10 μg/kg leptin (leptin group) or 2 mL saline (AP group) after cerulein injections. In the sham group,animals were given a single i.p. injection of 2 mL saline. Experimental samples were collected for biochemical and histological evaluations at 24 h and 48 h after the induction of AP or saline administration. Blood samples were obtained for the determination of amylase,lipase,tumor necrosis factor (TNF)-a,interleukin (IL)-1β,macrophage inflammatory peptide (MIP)-2 and soluble intercellular adhesion molecule (sICAM)-1 levels,while pancreatic and lung tissues were removed for myeloperoxidase (MPO) activity,nitric oxide (NOx) level,CD40 expression and histological evaluation. RESULTS:Cerulein injection caused severe AP,confirmed by an increase in serum amylase and lipase levels,histopathological findings of severe AP,and pancreatic MPO activity,compared to the values obtained in the sham group. In the leptin group,serum levels of MIP-2,sICMA-1,TNF-a,and IL-1b,pancreatic MPO activity,CD40 expression in pancreas and lung tissues,and NOx level in the lung tissue were lower compared to those in the AP group. Histologically,pancreatic and lungdamage was less severe following leptin administration. CONCLUSION:Exogenous leptin attenuates inflammatory changes,and reduces pro-inflammatory cytokines,nitric oxide levels,and CD40 expression in ceruleininduced AP and may be protective in AP associated ALI. 展开更多
关键词 LEPTIN Acute pancreatitis lung injury CD40 CYTOKINES
下载PDF
Therapeutic effects of Caspase-1 inhibitors on acute lung injury in experimental severe acute pancreatitis 被引量:26
11
作者 Xiao-Hua Zhang Ren-Min Zhu Wen-An Xu Hai-Jun Wan Heng Lu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第4期623-627,共5页
AIM: To assess the therapeutic effect of Caspase-1 inhibitors (ICE-I) on acute lung injury (ALI) in experimental severe acute pancreatitis (SAP). METHODS: Forty-two SD rats were randomly divided into 3 groups... AIM: To assess the therapeutic effect of Caspase-1 inhibitors (ICE-I) on acute lung injury (ALI) in experimental severe acute pancreatitis (SAP). METHODS: Forty-two SD rats were randomly divided into 3 groups: healthy controls (HC, n = 6); SAP-S group (n = 18); SAP-ICE-i group (n = 18). SAP was induced by retrograde infusion of 5% sodium taurocholate into the bile-pancreatic duct. HC rats underwent the same surgical procedures and duct cannulation without sodium taurocholate infusion, in SAP-S group, rats received the first intraperitoneal injection of isotonic saline 2 h after induction of acute pancreatitis and a repeated injection after 12 h. In SAP-ICE-I group, the rats were firstly given ICE inhibitors intraperitoneally 2 h after induction of pancreatitis. As in SAP-S group, the injection was repeated at 12 h. Serum 1L-1β was measured by EUSA. Intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were detected by semi-quantitative RT-PCR. The wet/dry weight ratios and histopathological changes of the lungs were also evaluated. RESULTS: Serum IL-1β levels in SAP-S group were 276.77 ± 44.92 pg/mL at 6 h, 308.99 ± 34.95 pg/mL at 12 h, and 311.60 ± 46.51 pg/mL at 18 h, which were increased significantly (P 〈 0.01, vs HC). in SAP- ICE-I group, those values were decreased significantly (P 〈 0.01, vs SAP-S). intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were observed in the HC group, while they were increased significantly in the SAP-S group (P 〈 0.01, vs HC). The expression of IL-lβ and IL-18 mRNA were decreased significantly in the SAP- ICE-I group (P 〈 0.01, vs SAP-S), whereas Caspase-1 mRNA expression had no significant difference (P 〉 0.05). The wet/dry weight ratios of the lungs in the SAP-S group were increased significantly (P 〈 0.05 at 6 h, P 〈 0.01 at 12 h and 18 h, vs HC) and they were decreased significantly in the SAP-ICE-I group (P 〈 0.05, vs SAP-S).Caspase-1 inhibitors ameliorated the severity of ALl in SAP.CONCLUSION: Caspase-1 activation, and overproduction of IL-1β and IL-18 play an important role in the course of ALI, and Caspase-1 inhibition is effective for the treatment of ALI in experimental SAP. 展开更多
关键词 Severe acute pancreatitis CASPASE-1 Interleukin-lβ INTERLEUKIN-18 Acute lung injury
下载PDF
Effect of nuclear factor kappa B on intercellular adhesion molecule-1 expression and neutrophil infiltration in lung injury induced by intestinal ischemia/reperfusion in rats 被引量:28
12
作者 Xiao-Feng Tian Ji-Hong Yao +4 位作者 Ying-Hua Li Xue-Song Zhang Bing-An Fen Chun-Ming Yang Shu-Sen Zheng 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第3期388-392,共5页
AIM: To investigate the role of nuclear factor kappa B (NF-κB) in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion (I/R), and its effect on intercellular adhesion molecule-1 (ICAM-1) ... AIM: To investigate the role of nuclear factor kappa B (NF-κB) in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion (I/R), and its effect on intercellular adhesion molecule-1 (ICAM-1) expression and neutrophil infiltration. METHODS: Twenty-four Wistar rats were divided randomly into control, I/R and pyrrolidine dithiocarbamate (PDTC) treatment groups, n = 8 in each. I/R group and PDTC treatment group received superior mysenteric artery (SMA) occluding for 1 h and reperfusion for 2 h. PDTC group was administrated with intraperitoneal injection of 2% 100 mg/kg PDTC 1 h before surgery. Lung histology and bronchia alveolus lung fluid (BALF) protein were assayed. Serum IL-6, lung malondialdehyde (MDA) and myeloperoxidase (MPO) as well as the expression level of NF-κB and ICAM-1 were measured.RESULTS: Lung injury induced by intestinal I/R, was characterized by edema, hemorrhage and neutrophil infiltration as well as by the significant rising of BALF protein. Compared to control group, the levels of serum IL-6 and lung MDA and MPO increased significantly in I/R group (P=0.001). Strong positive expression of NF-κB p65 and ICAM-1 was observed. After the administration of PDTC, the level of serum IL-6, lung MDA and MPO as well as NF-κB and ICAM-1 decreased significantly (P〈 0.05) when compared to I/R group.CONCLUSION: The activation of NF-κB plays an important role in the pathogenesis of lung injury induced by intestinal I/R through upregulating the neutrophil infiltration and lung ICAM-1 expression. PDTC as an inhibitor of NF-κB can prevent lung injury induced by intestinal I/R through inhibiting the activity of NF-κB. 展开更多
关键词 lung injury Intestinal ischemia/reperfusion NF-ΚB ICAM-1 Neutrophil infiltration
下载PDF
Role of Kupffer cells in acute hemorrhagic necrotizing pancreatitis-associated lung injury of rats 被引量:30
13
作者 Hong-Bin Liu Nai-Qiang Cui +1 位作者 Dong-Hua Li Chang Chen 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第3期403-407,共5页
AIM: To investigate the role of Kupffer cells (KCs) in acute hemorrhagic necrotizing pancreatitis-associated lung injury (AHNP-U). METHODS: Forty-two rats were allocated to four groups [sham operation, AHNP mode... AIM: To investigate the role of Kupffer cells (KCs) in acute hemorrhagic necrotizing pancreatitis-associated lung injury (AHNP-U). METHODS: Forty-two rats were allocated to four groups [sham operation, AHNP model, gadolinium chloride (GdCl3) pretreatment, GdCl3 control]. In GdCl3 pretreatment group, GdCl3 was administered by caudal vein injection 24 h before the AHNP model induction. Blood from the iliac artery, alveolar macrophages and tissues from the pancreas and lung, were collected in six animals per group 3 and 6 h after acute pancreatitis induction. TNF-α, IL-1 of Lserum, myeloperoxidase (MPO) of lung tissue, NF-κB activation of alveolar macrophages were detected. Serum AST and ALT in sham operation group and GdCl3 control group were tested. In addition, histopathological changes of the pancreas and lung were observed under light microscope. RESULTS: MPO of lung tissue and TNF-α, IL-1 levels of serum were all reduced significantly in GdCl3 pretreatment group compared to those in AHNP group (P〈0.01). NF-KB activation of alveolar macrophages was also attenuated significantly in GdCl3 pretreatment group compared to that in AHNP group (P〈0.01). The pathological injury of the lung was ameliorated obviously in GdCl3 pretreatment group compared to that in AHNP group. Nevertheless, the serum amylase level did not reduce and injury of the pancreas was not prevented in GdCl3 pretreatment group. CONCLUSION: Pulmonary injury induced by AHNP is mediated by KC activation and AHNP-LI can be significantly ameliorated by pretreatment with GdCh and KCs play a vital role in AHNP-LI. 展开更多
关键词 Pancreatitis-associated lung injury Kupffer cell NF-ΚB Gadolinium chloride
下载PDF
Dexmedetomidine Alleviates Pulmonary Edema by Upregulating AQP1 and AQP5 Expression in Rats with Acute Lung Injury Induced by Lipopolysaccharide 被引量:30
14
作者 姜远旭 戴中亮 +3 位作者 张雪萍 赵伟 黄强 高利昆 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2015年第5期684-688,共5页
This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five gr... This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five groups: normal saline control (NS) group, receiving intravenous 0.9% normal saline (5 mL/kg); LPS group, receiving intravenous LPS (10 mg/kg); small-dose dexmedetomidine (S) group, treated with a small dose of dexmedetomidine (0.5 μg·kg^-1·h^-1); medium-dose dexmedetomidine (M) group, treated with a medium dose of dexmedetomidine (2.5 μg·kg^-1·h^-1); high-dose dexmedetomidine (H) group, treated with a high dose of dexmedetomidine (5μg·kg^-1·h^-1). The rats were sacrificed 6 h after intravenous injection of LPS or NS, and the hmgs were removed for evaluating histological characteristics and determining the lung wet/dry weight ratio (W/D). The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the lung tissues were assessed by enzyme-linked immunosorbent assay (ELISA). The mRNA and protein expression levels of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) were detected by RT-PCR, immunohistochemistry, and Western blot- ting. The lung tissues from the LPS groups were significantly damaged, which were less pronounced in the H group but not in the small-dose dexmedetomidine group or medium-dose dexmedetomidine group. The W/D and the concentrations of TNF-α and IL-1β in the pulmonary tissues were increased in the LPS group as compared with those in NS group, which were reduced in the H group but not in S group or M group (P〈0.01). The expression of AQP1 and AQP5 was lower in the LPS group than in the NS group, and significantly increased in the H group but not in the S group or M group (P〈0.01). Our findings suggest that dexmedetomidine may alleviate pulmonary edema by increasing the expression of AQP-1 and AQP-5. 展开更多
关键词 DEXMEDETOMIDINE acute lung injury lung edema AQUAPORIN-1 AQUAPORIN-5
下载PDF
Circulating miRNAs as biomarkers for severe acute pancreatitis associated with acute lung injury 被引量:22
15
作者 Xiao-Guang Lu Xin Kang +3 位作者 Li-Bin Zhan Li-Min Kang Zhi-Wei Fan Li-Zhi Bai 《World Journal of Gastroenterology》 SCIE CAS 2017年第41期7440-7449,共10页
AIM To identify circulating micro(mi)RNAs as biological markers for prediction of severe acute pancreatitis(SAP) with acute lung injury(ALI).METHODS Twenty-four serum samples were respectively collected and classified... AIM To identify circulating micro(mi)RNAs as biological markers for prediction of severe acute pancreatitis(SAP) with acute lung injury(ALI).METHODS Twenty-four serum samples were respectively collected and classified as SAP associated with ALI and SAP without ALI, and the mi RNA expression profiles were determined by microarray analysis. These mi RNAs were validated by quantitative reverse transcriptionpolymerase chain reaction, and their putative targets were predicted by the online software Target Scan, mi Randa and Pic Tar database. Gene ontology(GO) and Kyoto encyclopedia of genes and genomes(commonly known as KEGG) were used to predict their possible functions and pathways involved.RESULTS We investigated 287 mi RNAs based on microarray data analysis. Twelve mi RNAs were differentially expressed in the patients with SAP with ALI and those with SAP without ALI. Hsa-mi R-1260 b, 762, 22-3 p, 23 b and 23 a were differently up-regulated and hsa-mi R-550 a*, 324-5 p, 484, 331-3 p, 140-3 p, 342-3 p and 150 were differently down-regulated in patients with SAP with ALI compared to those with SAP without ALI. In addition, 85 putative target genes of the significantly dysregulated mi RNAs were found by Target Scan, mi Randa and Pic Tar. Finally, GO and pathway network analysis showed that they were mainly enriched in signal transduction, metabolic processes, cytoplasm and cell membranes.CONCLUSION This is the first study to identify 12 circulating mi RNAs in patients with SAP with ALI, which may be biomarkers for prediction of ALI after SAP. 展开更多
关键词 MIRNAS Severe acute pancreatitis Acute lung injury BIOMARKER Microarray analysis
下载PDF
The role of Toll-like receptors in non-infectious lung injury 被引量:17
16
作者 Dianhua Jiang Jiurong Liang +1 位作者 Yuhang Li Paul W Noble 《Cell Research》 SCIE CAS CSCD 2006年第8期693-701,共9页
The role of Toll-like receptors (TLRs) in pathogen recognition has been expeditiously advanced in recent years. However, investigations into the function of TLRs in non-infectious tissue injury have just begun. Prev... The role of Toll-like receptors (TLRs) in pathogen recognition has been expeditiously advanced in recent years. However, investigations into the function of TLRs in non-infectious tissue injury have just begun. Previously, we and others have demonstrated that fragmented hyaluronan (HA) accumulates during tissue injury. CD44 is required to clear HA during tissue injury, and impaired clearance of HA results in unremitting inflammation. Additionally, fragmented HA stimulates the expression of inflammatory genes by inflammatory cells at the injury site. Recently, we identified that HA fragments require both TLR2 and TLR4 to stimulate mouse macrophages to produce inflammatory chemokines and cytokines. In a non-infectious lung injury model, mice deficient in both TLR2 and TLR4 show an impaired transepithelial migration of inflammatory cells, increased tissue injury, elevated lung epithelial cell apoptosis, and decreased survival. Lung epithelial cell overexpression of high molecular mass HA protected mice against acute lung injury and apoptosis, in part through TLR-dependent basal activation of NF-κB. The exaggerated injury in TLR2 and TLR4 deficient mice appears to be due to impaired HA-TLR interactions on epithelial cells. These studies identify that host matrix component HA and TLR interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity, and promote recovery from acute lung injury. 展开更多
关键词 Toll-like receptors HYALURONAN lung injury INFLAMMATION APOPTOSIS
下载PDF
Effect of resveratrol on microcirculation disorder and lung injury following severe acute pancreatitis in rats 被引量:19
17
作者 YongMeng MeiZhang +2 位作者 JunXu Xue-MinLiu Qing-YongMa 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第3期433-435,共3页
AIM: To investigate the mechanism of resveratrol underlying the microcirculation disorder and lung injury following severe acute pancreatitis (SAP). METHODS: Twenty-four rats were divided into 3 groups (SAP, sham and ... AIM: To investigate the mechanism of resveratrol underlying the microcirculation disorder and lung injury following severe acute pancreatitis (SAP). METHODS: Twenty-four rats were divided into 3 groups (SAP, sham and resveratrol groups) randomly. SAP model was established by injecting 4% sodium taurocholate l mL/kg through puncturing pancreatic ducts. Sham (control) group (8 rats) was established by turning over the duodenum. Resveratrol was given at 0.1 mg/kg b.m. intraperitoneally. Rats were sacrificed 9 h after SAP was induced. Blood samples were obtained for hemorrheological examination. Lung tissues were used for pathological observation, and examination of microvascular permeability, dry/wet ratio and myeloperoxidase (MPO) activity. Gene expression of intercellular adhesion molecule-1 (ICAM-1) was detected by RT-PCR. RESULTS: Compared with SAP group, resveratrol relieved the edema and infiltration of leukocytes in the lungs. Resveratrol improved markers of hemorrheology: high VTB (5.77±1.18 mPas vs9.49±1.34 mPas), low VTB (16.12±3.20 mPas vs30.91±7.28 mPas), PV (4.69±1.68 mPas vs 8.00±1.34 mPas), BSR (1.25±0.42 mm/h vs50.03±0.03 mm/h), VPC (54.67±3.08% vs 62.17±3.39%), fibrinogen (203.2?7.8 g/ L vs 51.3±19.1 g/L), original hemolysis (0.45±0.02 vs 0.49±0.02), and complete hemolysis (0.41±0.02 vs 0.43±0.02) (P<0.05). Resveratrol decreased the OD ratio of ICAM-1 gene (0.800±0.03 vs 1.188±0.10), dry/wet ratio (0.74±0.02 vs 0.77±0.03), microvascular permeability (0.079±0.006 vs 0.112±0.004) and MPO activity (4.42±0.32 vs 5.03±0.51) significantly (P<0.05). CONCLUSION: Resveratrol can improve the microcirculation disorder of the lung by decreasing leukocyte-endothelial interaction, reducing blood viscosity, improving the decrease of blood flow, and stabilizing erythrocytes in SAP rats. It may be a potential candidate to treat SAP and its severe complications (ALI). 展开更多
关键词 Severe acute pancreatitis RESVERATROL lung injury Micro-circulation disorder
下载PDF
Synergistic protection of astragalus polysaccharides and matrine against ulcerative colitis and associated lung injury in rats 被引量:25
18
作者 Xin Yan Qing-Ge Lu +4 位作者 Li Zeng Xiao-Hai Li Yu Liu Xue-Feng Du Guo-Min Bai 《World Journal of Gastroenterology》 SCIE CAS 2020年第1期55-69,共15页
BACKGROUND Ulcerative colitis(UC)is a main form of inflammatory bowel disease.Due to complicated etiology and a high rate of recurrence,it is quite essential to elucidate the underlying mechanism of and search for eff... BACKGROUND Ulcerative colitis(UC)is a main form of inflammatory bowel disease.Due to complicated etiology and a high rate of recurrence,it is quite essential to elucidate the underlying mechanism of and search for effective therapeutic methods for UC.AIM To investigate the effects of astragalus polysaccharides(APS)combined with matrine on UC and associated lung injury.METHODS UC was induced in rats by colon mucosal tissue sensitization combined with trinitro-benzene-sulfonic acid-ethanol.Then,the effects of the treatments of salazopyrine,APS,matrine,and APS combined with matrine on histopathological changes of lung and colon tissues,disease activity index(DAI),colon mucosal damage index(CMDI),serum endotoxin(ET)level,serum diamine oxidase(DAO)activity,the contents of tumor necrosis factor-αand interleukin-1β,and the activities of myeloperoxidase,superoxide dismutase,and malondialdehyde in lung tissues,as well as the protein expression of zonula occludens(ZO)-1,Occludin,and trefoil factor 3(TFF3)were detected in UC rats.RESULTS The treatments of salazopyrine,APS,matrine,and APS combined with matrine reduced DAI scores and improved histopathological changes of colon and lung tissues,as well as decreased CMDI scores,ET levels,and DAO activities in UC rats.Moreover,in lung tissues,inflammatory response and oxidative stress injury were relieved after the treatments of salazopyrine,APS,matrine,and APS combined with matrine in UC rats.Furthermore,the expression of ZO-1,Occludin,and TFF3 in lung and colon tissues was increased after different treatments in UC rats.Notably,APS combined with matrine exerted a better protective effect against UC and lung injury compared with other treatments.CONCLUSION APS combined with matrine exert a synergistic protective effect against UC and lung injury,which might be associated with regulating TFF3 expression. 展开更多
关键词 Astragalus polysaccharides MATRINE Ulcerative colitis lung injury Trinitrobenzene-sulfonic acid-ethanol Trefoil factor 3
下载PDF
Melatonin attenuates acute pancreatitis-associated lung injury in rats by modulating interleukin 22 被引量:12
19
作者 Jia-Ping Huai Xue-Cheng Sun Meng-Jun Chen Yin Jin Xiao-Hua Ye Jian-Sheng Wu Zhi-Ming Huang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第36期5122-5128,共7页
AIM: To investigate whether therapeutic treatment with melatonin could protect rats against acute pan- creatitis and its associated lung injury. METHODS: Seventy-two male Sprague-Dawley rats were randomly divided in... AIM: To investigate whether therapeutic treatment with melatonin could protect rats against acute pan- creatitis and its associated lung injury. METHODS: Seventy-two male Sprague-Dawley rats were randomly divided into three groups: the sham op- eration (SO), severe acute pancreatitis (SAP), and mel- atonin treatment (MT) groups. Acute pancreatitis was induced by infusion of 1 mL/kg of sodium taurocholate (4% solution) into the biliopancreatic duct. Melatonin (50 mg/kg) was administered 30 min before pancre- atitis was induced, and the severity of pancreatic and pulmonary injuries was evaluated 1, 4 and 8 h after induction. Serum samples were collected to measure amylase activities, and lung tissues were removed to measure levels of mRNAs encoding interleukin 22 (IL-22) and T helper cell 22 (Th22), as well as levels of IL-22.ing IL-22 and Th22 were significantly higher (P 〈 0.001) in the MT group than in the SAP group (0.526 ± 0.143 vs 0.156 ± 0.027, respectively, here and throughout, after 1 h; 0.489 ± 0.150 vs 0.113 ± 0.014 after 4 h; 0.524 ± 0.168 vs 0.069 ± 0.013 after 8 h, 0.378 ± 0.134 vs 0.122 ± 0.015 after 1 h; 0.205 ± 0.041 vs 0.076 ± 0.019 after 4 h; 0.302 ± 0.108 vs 0.045 ± 0.013 after 8 h, respectively) and significantly lower (P 〈 0.001) in the SAP group than in the SO group (0.156 ± 0.027 vs 1.000 ± 0.010 after 1 h; 0.113 ± 0.014 vs 1.041 ± 0.235 after 4 h; 0.069 ± 0.013 vs 1.110 ± 0.213 after 8 h, 0.122 ± 0.015 vs 1.000 ± 0.188 after 1 h; 0.076 ± 0.019 vs 0.899 ± 0.125 after 4 h; 0.045 ± 0.013 vs 0.991 ± 0.222 after 8 h, respectively). The mean pathologi- cal scores for pancreatic tissues in the MT group were significantly higher (P 〈 0.01) than those for samples in the SO group (1.088 ± 0.187 vs 0.488 ± 0.183 after 1 h, 2.450 ± 0.212 vs 0.469 ± 0.242 after 4 h; 4.994 ± 0.184 vs 0.513 ± 0.210 after 8 h), but were significantly lower (P 〈 0.01) than those for samples in the SAP group at each time point (1.088 ± 0.187 vs 1.969 ± 0.290 after 1 h; 2.450 ± 0.212 vs 3.344 ± 0.386 after 4 h; 4.994 ± 0.184 vs 6.981 ± 0.301 after 8 h). The severity of SAP increased significantly (P 〈 0.01) over time in the SAP group (1.088 ± 0.187 vs 2.450 ± 0.212 between 1 h and 4 h after inducing pancreatitis; and 2.450 ± 0.212 vs 4.994 ± 0.184 between 4 and 8 h after inducing pan- creatitis). CONCLUSION: Melatonin protects rats against acute pancreatitis-associated lung injury, probably through the upregulation of IL-22 and Th22, which increases the innate immunity of tissue cells and enhances their regeneration. 展开更多
关键词 Interleukin 22 MELATONIN Pancreatitis-associated lung injury Severe acute pancreatitis Thelper 22 cell
下载PDF
Microcirculation disturbance affects rats with acute severe pancreatitis following lung injury 被引量:17
20
作者 Xue-Min Liu Qing-Guang Liu Jun Xu Cheng-En Pan 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第39期6208-6211,共4页
AIM: To study the effects of microcirculation disturbance(MD) on rats with acute severe pancreatitis (ASP).METHODS: We developed ASP rat models, and anatomized separately after 1, 3, 5, 7, and 9 h. We took out blood a... AIM: To study the effects of microcirculation disturbance(MD) on rats with acute severe pancreatitis (ASP).METHODS: We developed ASP rat models, and anatomized separately after 1, 3, 5, 7, and 9 h. We took out blood and did hemorrheologic examination and erythrocyte osmotic fragility test, checked up the water content, capillary permeability, and genetic expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissues, examined the apoptosis degree of blood vessel endothelium while we tested related gene expression of Bax and Bcl-2in lung tissues. We did the same examination in control group.RESULTS: The viscosity of total blood and plasma, the hematocrit, and the erythrocyte osmotic fragility were all increased. Fibrinogen was decreased. The water content in lung tissues and capillary permeability were increased.Apoptosis degree of blood vessel endothelium was increased too. ICAM-1 genetic expression moved up after1 h and reached its peak value after 9 h.CONCLUSION: MD plays an important role in ASP following acute lung injury (ALI). The functional damage of blood vessel endothelium, the apoptosis of capillary vessel endothelium, WBC edging-concentration and the increasing of erythrocyte fragility are the main reasons of ALI. 展开更多
关键词 MICROCIRCULATION Acute pancreatitis lung injury
下载PDF
上一页 1 2 15 下一页 到第
使用帮助 返回顶部