Creatinine accelerates APAP-induced liver damage by increasing oxidative stress through ROS/JNK signaling pathway.

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作者： Fang,Liu ^[1] ; Yan,Liu ^[2] ; Qifeng,Peng ^[3] ; Guodong,Wang ^[3] ; Qing,Tan ^[1] ; Zhongyue,Ou ^[4] ; Qishan,Xu ^[1] ; Chixiang,Liu ^[1] ; Daming,Zuo ^[2] ; Jianbo,Zhao ^[5]

作者单位： Division of Vascular and Interventional Radiology, Department of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. ^[1] Department of Medical Laboratory, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China. ^[2] Syndrome Laboratory of Integrated Chinese and Western Medicine, School of Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China. ^[3] Department of Oncology, Liuzhou Workers Hospital, Liuzhou, China. ^[4] Department of Blood Transfusion, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. ^[5] Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China. ^[6]

关键词 C-jun N-terminal kinase acetaminophen creatinine hepatotoxicity reactive oxygen species

DOI 10.3389/fphar.2022.959497

PMID 36091804

发布时间 2022-09-13

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Frontiers in pharmacology

2022年13卷

959497页

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Creatinine accelerates APAP-induced liver damage by increasing oxidative stress through ROS/JNK signaling pathway.

Frontiers in pharmacology

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Frontiers in pharmacology

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Creatinine accelerates APAP-induced liver damage by increasing oxidative stress through ROS/JNK signaling pathway.

Frontiers in pharmacology

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Frontiers in pharmacology

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