Ablation of apoptosis-stimulating of p53 protein 1 protects mice from acute hepatic injury and dysfunction via NF-κB pathway in CCl4-induced hepatotoxicity
Tolessa Muleta Daba1
Xiang Huang2
Timur Yagudin2
Ying Yang2
Jiangang Wang3
Xiaoyu Fu2
Yue Zhao2
Haiyu Gao2
Yang Zhou2
Zhenwei Pan4
Xiangyu Zhong3
1.Department of Pharmacology,College of Pharmacy,Harbin Medical University,Harbin,150081,China;Department of Biochemistry and Molecular Biology,College of Basic Medical Sciences,Harbin Medical University,Harbin,150081,China;Department of Biology,College of Natural and Computational Sciences,Buie Hora University,Buie Hora,Oromia,Ethiopia,P.O.Box:1442.Department of Pharmacology,College of Pharmacy,Harbin Medical University,Harbin,150081,China3.Department of Hepatopancreatobiliary Surgery,Second Affiliated Hospital of Harbin Medical University,Harbin,China4.Department of Pharmacology,College of Pharmacy,Harbin Medical University,Harbin,150081,China;Research Unit of Noninfectious Chronic Diseases in Frigid Zone,Chinese Academy of Medical Sciences,2019RU070
摘要：Acute liver injury(ALI)is characterized by apoptosis,inflammation,and oxidative stress,and pathogenic mechanism of ALI is poorly understood.Apoptosis-stimulating of p53 protein 1(ASPP1)is involved in environmental responses,tumor growth,and NF-κB activity,which is of critical importance to ALI.However,the role of ASPP1 in ALI remains largely unexplored.The current study aimed to determine the role of ASPP1 in ALI induced by CCl4 and the underlying mechanism.ASPP1 expression was detected in wild type(WT)mice with ALI induced by CCl4.The function of ASPP1 in ALI induced by CCl4 was investigated using conventional knockout ASPP1 mice.ASPP1 expression significantly increased in ALI mice at 24 hours after CCl4 injection.Deletion of ASSP1 ameliorated apoptosis,inflammation,and necrosis in ALI relative to WT mice.In addition,deficiency of ASPP1 improved liver flood flow as well as ALT and AST levels.The levels of phosphorylated p65 and phosphorylated IκBα were lower in ASPP1-/-mice than in WT mice with ALI.These results implicate that deletion of ASPP1 may act via inhibition of the NF-κB pathway and protect mice from ALI,which may be a new potential therapeutic target for the treatment of ALI.
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论文发表日期：2021-01-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：12( 53-64 )
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