Glucosamine attenuates alcohol-induced acute liver injury via inhibiting oxidative stress and inflammation

Weiwen Lai; Shipeng Zhou; Yan Bai; Qishi Che; Hua Cao; Jiao Guo; Zhengquan Su

doi:10.1016/j.crfs.2024.100699

Glucosamine attenuates alcohol-induced acute liver injury via inhibiting oxidative stress and inflammation

Curr Res Food Sci. 2024 Feb 16:8:100699. doi: 10.1016/j.crfs.2024.100699. eCollection 2024.

Authors

Weiwen Lai^{1

2}, Shipeng Zhou^{1

2}, Yan Bai³, Qishi Che⁴, Hua Cao⁵, Jiao Guo², Zhengquan Su¹

Affiliations

¹ Guangdong Engineering Research Center of Natural Products and New Drugs, Guangdong Provincial University Engineering Technology Research Center of Natural Products and Drugs, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
² Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
³ School of Public Health, Guangdong Pharmaceutical University, Guangzhou, 510310, China.
⁴ Guangzhou Rainhome Pharm & Tech Co., Ltd, Science City, Guangzhou, 510663, China.
⁵ School of Chemistry and Chemical Engineering, Guangdong Pharmaceutical University, Zhongshan, 528458, China.

Abstract

Alcohol liver disease (ALD) is a liver disease caused by long-term heavy drinking. Glucosamine (GLC) is an amino monosaccharide that plays a very important role in the synthesis of human and animal cartilage. GLC is commonly used in the treatment of mild to moderate osteoarthritis and has good anti-inflammatory and antioxidant properties. In this study, alcoholic injury models were constructed in mice and human normal hepatocyte L02 cells to explore the protective effect and mechanism of GLC on ALD. Mice were given GLC by gavage for 30 days. Liver injury models of both mice and L02 cells were produced by ethanol. Detecting the levels of liver injury biomarkers, lipid metabolism, oxidative stress biomarkers, and inflammatory factors through different reagent kits. Exploring oxidative and inflammatory pathways in mouse liver tissue through Western blot and RT-PCR. The results showed that GLC can significantly inhibit the abnormal increase of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), triglycerides (TG), total cholesterol (TC), very low density lipoprotein (VLDL), low-density lipoprotein cholesterol (LDL-C), and can significantly improve the level of high-density lipoprotein cholesterol (HDL-C). In addition, GLC intervention significantly improved alcohol induced hepatic oxidative stress by reducing the levels of malondialdehyde (MDA) and, increasing the levels of glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) in the liver. Further mechanisms suggest that GLC can inhibit the expression of ethanol metabolism enzyme cytochrome P4502E1 (CYP2E1), activate the antioxidant pathway Keap1/Nrf2/HO-1, down-regulate the phosphorylation of MAPK and NF-κB signaling pathways, and thus reduce the expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Therefore, GLC may be a significant candidate functional food for attenuating alcohol induced acute liver injury.

Keywords: Alcoholic liver disease (ALD); Anti-inflammatory; Antioxidation; Glucosamine; Hepatoprotective.