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Proanthocyanidin Alleviates liver ischemia/reperfusion injury by Suppressing Autophagy and Apoptosis via the􀀳􀀳􀀤􀀵􀄮􀀒􀀳􀀪􀀦􀀔􀄮􀀃􀀶􀁌􀁊􀁑􀁄􀁏􀁌􀁑􀁊􀀃􀀳􀁄􀁗􀁋􀁚􀁄􀁜

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Journal of Clinical and Translational Hepatology 2023年第6期11卷 1329-1340页

作者： Zhilu Yao Ning Liu Hui Lin Yingqun Zhou Department of Gastroenterology Jingan District Zhabei Central HospitalShanghaiChina Clinical Medical College of Shanghai Tenth People’s Hospital Nanjing Medical UniversityNanjingJiangsuChina Department of Gastroenterology Changzhou Maternal and Child Health HospitalChangzhouJiangsuChina Department of Gastroenterology Shanghai Tenth People’s HospitalTongji University School of MedicineShanghaiChina

Background and Aims:Hepatic ischemia-reperfusion injury(IRI)is a common pathophysiological phenomenon in clinical practice,which usually occurs in liver transplantation,liver resection,severe trauma,and hemorrhagic ***(PC),exerted from various plants with antioxidant,antitumor,and antiaging activity,were administrated in our study to investigate the underlying mechanism of its protective function on ***:Two doses of PC(50 mg/kg,100 mg/kg)were given to BALB/c mice by intragastric administration for 7 days before partial(70%)warm IR *** and liver tissues were collected 2,8,and 24 h after reperfusion for relevant ***:The results of transaminase and hematoxylin and eosin staining indicated that PC pretreatment significantly alleviated IRI in *** total superoxide dismutase increased and malondialde-hyde decreased in PC pretreatment ***-linked immunosorbent assays,western blotting,quantitative real-time polymerase chain reaction,and immunohistochemistry showed that inflammation,apoptosis,and autophagy in PC preprocessing groups were significantly inhibited and were *** protein,mRNA expression,and immunohistochemical staining results of peroxisome proliferator-activated receptor alpha(PPARa)and peroxisome proliferator-activated receptor gamma coactivator 1-alpha(PGC1a)in the PC pretreatment groups were significantly upregulated compared with the IR group in a dose-dependent ***:PC pretreatment suppressed inflammation,apoptosis,and autophagy via the PPAR-α signaling pathway to protect against IRI of the liver in mice.

关键词： liver ischemia/reperfusion injury Proanthocyanidin Apoptosis Autophagy PPARa PGC1α

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Hyperglycemia Triggered ATF6-CHOP Pathway Exacerbates liver ischemia/reperfusion injury:Immunomodulation by Regulatingβ-catenin signaling

Hyperglycemia Triggered ATF6-CHOP Pathway Exacerbates Liver ...

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第十二届全国免疫学学术大会

作者： Yang Chao Cheng Feng Hu Yuanchang Lu Ling Rao Jianhua Wang Xuehao the First Affiliated Hospital of Nanjing Medical University

Hyperglycemia is an adverse factor of hepatic ischemia reperfusion injury(IRI)during liver transpIantation or hepatectomy,but the underlying mechanism has not been *** previous studies have demonstrated endoplasmic re... 详细信息

关键词： Hyperglycemia ATF6 CHOP β-catenin liver ischemia/reperfusion injury

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TGR5 protects liver ischemia reperfusion injury through reducing macrophage mobility and polarization via AMPK/mTORC1 axis signaling

TGR5 protects liver ischemia reperfusion injury through redu...

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第十二届全国免疫学学术大会

作者： Zhou Shun Zhang Feng Lv Ling Zhou Haoming Jiang Su province hospital

Background The plasma membrane bound G protein-coupled bile acid receptor(TGR5) is involved in several metabolic processes,and protective roles of TGR5 have been found in liver ischemia/reperfusion injury(IRI).However,the underlying mechanism still remains to be further *** study aimed at investigating the role of TGR5 in regulation of macrophage migration and polarization during liver *** WT and TGR5 KO mice were subjected to liver partial warm ischemia/reperfusion *** injuries and macrophage-related inflammation were compared between *** of intrahepatic macrophages in IR livers were calculated by immunohistochemical *** vitro,macrophage migration,M1/M2 polarization and the underlying mechanisms were also studied using bone-marrow-derived macrophages(BMDMs) isolated from WT and TGR5 *** The serum ALT and AST levels,intrahepatic inflammation and hepatocytes apoptosis were markedly increased in the TGR5 KO *** with TGR5 agonist INT-777 in vivo protected liver IRI in WT mice,but with no significant effects in TGR5 KO *** frequency of CD11 b+macrophage were increased in TGR5 KO ischemic livers,while treatment with INT-777 decreased CD11 b+ *** vitro,TGR5 KO BMDMs had enhanced ability of migration as compare to WT *** p-AMPK and decreased p-mTORC1 was found in TGR5 KO BMDMs after LPS *** siRNA treatment enhanced mTORC1 activation and abrogated the enhanced mobility in TGR5 KO BMDMs,indicating the critical roles of TGR5/AMPK/mTORC1 in regulating the macrophage ***5 promoted M2 polarization as shown by increased Arg1 and PPARγ(M2),but deceased iNOS(M1) gene ***-777 treatment further enhanced WT BMDMs M2 polarization,but had no significant effects in TGR5 KO *** TGR5 protects liver ischemia/reperfusion injury through TGR5/AMPK/mTORC1 axis regulated macrophages migration and polarization.

关键词： liver ischemia/reperfusion injury TGR5 macrophage migration

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Ischemic preconditioning attenuates ischemia/reperfusion injury in rat steatotic liver:role of heme oxygenase-1-mediated autophagy

Ischemic preconditioning attenuates ischemia/reperfusion inj...

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第十一届全国免疫学学术大会

作者： Liu Anding Guo Enshuang Yang Jiankun Li Renlong Yang Yan Liu Shenpei Jiang Xiaojing Yang Dongliang Experimental Medicine Center Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Infectious Diseases Wuhan General Hospital of Guangzhou Military Command Department of Infectious Diseases Union HospitalTongji Medical CollegeHuazhong University of Science and Technology

Objective: Steatotic livers are more susceptible to ischemia/reperfusion(I/R) injury, which is ameliorated by ischemic preconditioning(IPC). Autophagy possesses protective action on liver I/R injury and declines in steatotic *** aim of this study was to test the hypothesis that the increased susceptibility of steatotic livers to I/R injury was associated with defective hepatic autophagy, which could be restored by IPC via heme oxygenase-1(HO-1) signaling. Methods: Obesity and hepatic steatosis was induced using a high fat *** livers and steatotic hepatocytes were subjected to in vivo and in vitro I/R, respectively. To evaluate the contribution of autophagy to the protective effect of IPC, Obese rats or steatotic hepatocytes were pretreated with 3-methyladenine or rapamycin. HO-1 or calpain 2 was blocked by tin protoporphyrin IX or N-acetyl-leucyl-leucyl-methioninal, respectively. Results: Obesity impaired hepatic autophagy activity and decreased hepatic HO-1 expression. Induction of HO-1 restored autophagy activity and inhibited calpain 2 activity. Additionally, suppression of calpain 2 activity also restored autophagy activity. Mitochondrial dysfunction and hepatocellular injury were significantly increased in steatotic livers compared to lean livers in response to I/R injury. This increase in sensitivity to I/R injury was associated with defective hepatic autophagy activity in steatotic livers. IPC increased autophagy and reduced mitochondrial dysfunction and hepatocellular damage in steatotic livers following I/R injury. Furthermore, IPC increased HO-1 expression. Inhibition of HO-1 decreased the IPC-induced autophagy, increased calpain 2 activity and diminished the protective effect of IPC against I/R injury. Inhibition of calpain 2 restored autophagic defect and attenuated mitochondrial dysfunction in steatotic livers after I/R. Conclusion: Collectively, IPC might ameliorate steatotic liver damage and restore mitochondrial function via HO-1-me

关键词： Ischemic preconditioning Steatosis liver ischemia/reperfusion injury Autophagy Heme oxygenase-1

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