<i>Lycium</i><i>barbarum</i> polysaccharides ameliorate canine acute liver injury by reducing oxidative stress, protecting mitochondrial function, and regulating metabolic pathways.

Jianjia Huang; Yuman Bai; Wenting Xie; Rongmei Wang; Wenyue Qiu; Shuilian Zhou; Zhaoxin Tang; Jianzhao Liao; Rongsheng SU

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Lyciumbarbarum polysaccharides ameliorate canine acute liver injury by reducing oxidative stress, protecting mitochondrial function, and regulating metabolic pathways.

Author: Jianjia HUANG ¹ ; Yuman BAI ¹ ; Wenting XIE ¹ ; Rongmei WANG ² ; Wenyue QIU ¹ ; Shuilian ZHOU ¹ ; Zhaoxin TANG ¹ ; Jianzhao LIAO ¹ ; Rongsheng SU ³
Author Information

1. College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
2. College of Biology and Agriculture, Shaoguan University, Shaoguan 512005, China.
3. College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China. srsh168@163.com.
Publication Type:Journal Article
Keywords: Acute liver injury; Lycium barbarum polysaccharides; Metabolomics; Mitochondrial dysfunction; Oxidative stress
MeSH: Animals; Dogs; Antioxidants/metabolism*; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury/drug therapy*; Kelch-Like ECH-Associated Protein 1/metabolism*; Liver; Metabolic Networks and Pathways; Mitochondria/metabolism*; NF-E2-Related Factor 2/metabolism*; Oxidative Stress; Polysaccharides/pharmacology*; Lycium/chemistry*
From: Journal of Zhejiang University. Science. B 2023;24(2):157-171
CountryChina
Language:English
Abstract: The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lyciumbarbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl₄). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl₄ solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl₄-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase II detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I‒V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.