Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα Pathway

Hepatic ischemia-reperfusion (IR) injury is a clinically significant process that frequently occurs in liver transplantation, partial hepatectomy, and hemorrhagic shock. The aim of this study was to explore the effectiveness of luteolin in hepatic IR injury and the underlying mechanism. BALB/c mice...

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Main Authors: Yuhui Jiang, Wenjuan Yang, Jiameng Ding, Jie Ji, Liwei Wu, Yuanyuan Zheng, Yan Li, Ziqi Cheng, Jie Zhang, Qiang Yu, Jiao Feng, Jingjing Li, Jianye Wu, Yingqun Zhou, Chuanyong Guo
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2022/8161946
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author Yuhui Jiang
Wenjuan Yang
Jiameng Ding
Jie Ji
Liwei Wu
Yuanyuan Zheng
Yan Li
Ziqi Cheng
Jie Zhang
Qiang Yu
Jiao Feng
Jingjing Li
Jianye Wu
Yingqun Zhou
Chuanyong Guo
author_facet Yuhui Jiang
Wenjuan Yang
Jiameng Ding
Jie Ji
Liwei Wu
Yuanyuan Zheng
Yan Li
Ziqi Cheng
Jie Zhang
Qiang Yu
Jiao Feng
Jingjing Li
Jianye Wu
Yingqun Zhou
Chuanyong Guo
author_sort Yuhui Jiang
collection DOAJ
description Hepatic ischemia-reperfusion (IR) injury is a clinically significant process that frequently occurs in liver transplantation, partial hepatectomy, and hemorrhagic shock. The aim of this study was to explore the effectiveness of luteolin in hepatic IR injury and the underlying mechanism. BALB/c mice were randomly divided into six groups, including normal controls (NC), luteolin (50 mg/kg), sham procedure, IR+25 mg/kg luteolin, and IR+50 mg/kg luteolin group. Serum and tissue samples were collected at 6 and 24 h after reperfusion to assay liver enzymes, inflammatory factors, expression of proteins associated with apoptosis and autophagy, and factors associated with the extracellular signal-regulated kinase/peroxisome proliferator-activated receptor alpha (ERK/PPARα) pathway. Luteolin preconditioning decreased hepatocyte injury caused by ischemia-reperfusion, downregulated inflammatory factors, and inhibited apoptosis and autophagy. Luteolin also inhibited ERK phosphorylation and activated PPARα.
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institution Kabale University
issn 1687-4765
language English
publishDate 2022-01-01
publisher Wiley
record_format Article
series PPAR Research
spelling doaj-art-e94db8358e7e468bbc538c04f89317282025-02-03T01:06:58ZengWileyPPAR Research1687-47652022-01-01202210.1155/2022/8161946Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα PathwayYuhui Jiang0Wenjuan Yang1Jiameng Ding2Jie Ji3Liwei Wu4Yuanyuan Zheng5Yan Li6Ziqi Cheng7Jie Zhang8Qiang Yu9Jiao Feng10Jingjing Li11Jianye Wu12Yingqun Zhou13Chuanyong Guo14Department of GastroenterologyDepartment of EmergencyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyHepatic ischemia-reperfusion (IR) injury is a clinically significant process that frequently occurs in liver transplantation, partial hepatectomy, and hemorrhagic shock. The aim of this study was to explore the effectiveness of luteolin in hepatic IR injury and the underlying mechanism. BALB/c mice were randomly divided into six groups, including normal controls (NC), luteolin (50 mg/kg), sham procedure, IR+25 mg/kg luteolin, and IR+50 mg/kg luteolin group. Serum and tissue samples were collected at 6 and 24 h after reperfusion to assay liver enzymes, inflammatory factors, expression of proteins associated with apoptosis and autophagy, and factors associated with the extracellular signal-regulated kinase/peroxisome proliferator-activated receptor alpha (ERK/PPARα) pathway. Luteolin preconditioning decreased hepatocyte injury caused by ischemia-reperfusion, downregulated inflammatory factors, and inhibited apoptosis and autophagy. Luteolin also inhibited ERK phosphorylation and activated PPARα.http://dx.doi.org/10.1155/2022/8161946
spellingShingle Yuhui Jiang
Wenjuan Yang
Jiameng Ding
Jie Ji
Liwei Wu
Yuanyuan Zheng
Yan Li
Ziqi Cheng
Jie Zhang
Qiang Yu
Jiao Feng
Jingjing Li
Jianye Wu
Yingqun Zhou
Chuanyong Guo
Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα Pathway
PPAR Research
title Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα Pathway
title_full Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα Pathway
title_fullStr Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα Pathway
title_full_unstemmed Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα Pathway
title_short Luteolin Pretreatment Attenuates Hepatic Ischemia-Reperfusion Injury in Mice by Inhibiting Inflammation, Autophagy, and Apoptosis via the ERK/PPARα Pathway
title_sort luteolin pretreatment attenuates hepatic ischemia reperfusion injury in mice by inhibiting inflammation autophagy and apoptosis via the erk pparα pathway
url http://dx.doi.org/10.1155/2022/8161946
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