2. Academic Validation
  3. Cyanidin-3-O-glucoside alleviates ethanol-induced liver injury by promoting mitophagy in a Gao-binge mouse model of alcohol-associated liver disease

Cyanidin-3-O-glucoside alleviates ethanol-induced liver injury by promoting mitophagy in a Gao-binge mouse model of alcohol-associated liver disease

  • Biochim Biophys Acta Mol Basis Dis. 2024 May 25;1870(6):167259. doi: 10.1016/j.bbadis.2024.167259.
Qiao He 1,  Zhaoqing Yin 1,  Yunling Chen 2,  Yunxiao Wu 1,  Di Pan 1,  Yuanhao Cui 2,  Zinuo Zhang 2,  Hanyu Ma 1,  Xuanji Li 1,  Chang Shen 1,  Junfang Qin 3,  Shuanglian Wang 4
Affiliations

Affiliations

  • 1 Department of Physiology and Pathophysiology, School of Basic Medical Science, Shandong University, Jinan, China.
  • 2 Science and Technology Innovation Center, Shandong First Medical University, Jinan, China.
  • 3 School of Medicine, Nankai University, Tianjin, China. Electronic address: qjf@nankai.edu.cn.
  • 4 Science and Technology Innovation Center, Shandong First Medical University, Jinan, China. Electronic address: wsl6319@sdu.edu.cn.
PMID: 38796918 DOI: 10.1016/j.bbadis.2024.167259
Abstract

Background: Alcohol-associated liver disease (ALD) is a leading cause of liver disease-related deaths worldwide. Unfortunately, approved medications for the treatment of this condition are quite limited. One promising candidate is the anthocyanin, Cyanidin-3-O-glucoside (C3G), which has been reported to protect mice against hepatic lipid accumulation, as well as fibrosis in different animal models. However, the specific effects and mechanisms of C3G on ALD remain to be investigated.

Experimental approach: In this report, a Gao-binge mouse model of ALD was used to investigate the effects of C3G on ethanol-induced liver injury. The mechanisms of these C3G effects were assessed using AML12 hepatocytes.

Results: C3G administration ameliorated ethanol-induced liver injury by suppressing hepatic oxidative stress, as well as through reducing hepatic lipid accumulation and inflammation. Mechanistically, C3G activated the AMPK pathway and enhanced Mitophagy to eliminate damaged mitochondria, thus reducing mitochondria-derived reactive oxidative species in ethanol-challenged hepatocytes.

Conclusions: The results of this study indicate that Mitophagy plays a potentially important role underlying the hepatoprotective action of C3G, as demonstrated in a Gao-binge mouse model of ALD. Accordingly, C3G may serve as a promising, new therapeutic drug candidate for use in ALD.

Keywords

AMPK pathway; Alcoholic liver disease; Cyanidin-3-O-glucoside; mitophagy.

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