Lai Weiwen, Zhou Shipeng, Bai Yan, Che Qishi, Cao Hua, Guo Jiao, Su Zhengquan
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.
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.
Curr Res Food Sci. 2024 Feb 16;8:100699. doi: 10.1016/j.crfs.2024.100699. eCollection 2024.
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.
酒精性肝病（ALD）是一种由长期大量饮酒引起的肝脏疾病。氨基葡萄糖（GLC）是一种氨基单糖，在人和动物软骨的合成中起着非常重要的作用。GLC常用于治疗轻至中度骨关节炎，具有良好的抗炎和抗氧化特性。在本研究中，在小鼠和人正常肝细胞L02细胞中构建酒精损伤模型，以探讨GLC对ALD的保护作用及机制。给小鼠灌胃GLC 30天。通过乙醇建立小鼠和L02细胞的肝损伤模型。使用不同的试剂盒检测肝损伤生物标志物、脂质代谢、氧化应激生物标志物和炎症因子的水平。通过蛋白质免疫印迹法（Western blot）和逆转录聚合酶链反应（RT-PCR）探索小鼠肝组织中的氧化和炎症途径。结果表明，GLC可显著抑制天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、碱性磷酸酶（ALP）、乳酸脱氢酶（LDH）、甘油三酯（TG）、总胆固醇（TC）、极低密度脂蛋白（VLDL）、低密度脂蛋白胆固醇（LDL-C）的异常升高，并可显著提高高密度脂蛋白胆固醇（HDL-C）水平。此外，GLC干预通过降低肝脏中丙二醛（MDA）水平、提高谷胱甘肽（GSH）、过氧化氢酶（CAT）和超氧化物歧化酶（SOD）水平，显著改善酒精诱导的肝脏氧化应激。进一步的机制表明，GLC可抑制乙醇代谢酶细胞色素P4502E1（CYP2E1）的表达，激活抗氧化途径Keap1/Nrf2/HO-1，下调丝裂原活化蛋白激酶（MAPK）和核因子κB（NF-κB）信号通路的磷酸化，从而降低肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的表达。因此，GLC可能是减轻酒精诱导的急性肝损伤的一种重要的功能性食品候选物。
