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- Title
Methyl 6-O-cinnamoyl-α- d -glucopyranoside Ameliorates Acute Liver Injury by Inhibiting Oxidative Stress Through the Activation of Nrf2 Signaling Pathway.
- Authors
Xu, Qianqian; Deng, Yanfang; Ming, Jiaxiong; Luo, Zengwei; Chen, Xia; Chen, Tianqi; Wang, Yafen; Yan, Shan; Zhou, Jiajun; Mao, Lina; Sun, Weiguang; Zhou, Qun; Ren, Hong; Zhang, Yonghui
- Abstract
Excessive stimulation of hepatotoxins and drugs often lead to acute liver injury, while treatment strategies for acute liver injury have been limited. Methyl 6-O-cinnamoyl-α-d-glucopyranoside (MCGP) is a structure modified compound from cinnamic acid, a key chemical found in plants with significant antioxidant, anti-inflammatory, and antidiabetic effects. In this study, we investigated the effects and underlying mechanisms of MCGP on acetaminophen (APAP)- or carbon tetrachloride (CCl4)-induced acute liver injury. As a result, MCGP inhibited cell death and apoptosis induced by APAP or CCl4, and suppressed the reactive oxygen species (ROS) generation stimulated by H2O2 in liver AML12 cells. In vivo , MCGP alleviated APAP/CCl4-induced hepatic necrosis and resumed abnormal aminotransferase activities and liver antioxidase activities. In addition, MCGP depressed APAP- or CCl4-induced oxidative stress through the suppression of CYP2E1 and activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. MCGP also enhanced the number of PCNA-positive hepatocytes, increased hepatic PCNA and Bcl-XL, and decreased BAX expression in APAP-/CCl4-intoxicated mice. Furthermore, MCGP activated the GSDMD-N/cleaved caspase 1 pathway. In summary, MCGP might act as a potential therapeutic drug against drug-induced and chemical-induced acute liver injuries, and its underlying mechanisms might engage on the pressing of oxidative stress, refraining of hepatocyte apoptosis, and facilitating of liver regeneration.
- Subjects
NUCLEAR factor E2 related factor; CELL death; LIVER injuries; HEPATOCYTE growth factor; OXIDATIVE stress; CELLULAR signal transduction
- Publication
Frontiers in Pharmacology, 2022, Vol 13, p1
- ISSN
1663-9812
- Publication type
Article
- DOI
10.3389/fphar.2022.873938