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

IF 6.2 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY
Weiwen Lai , Shipeng Zhou , Yan Bai , Qishi Che , Hua Cao , Jiao Guo , Zhengquan Su
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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.

Abstract Image

氨基葡萄糖通过抑制氧化应激和炎症减轻酒精引起的急性肝损伤
酒精肝(ALD)是一种由长期大量饮酒引起的肝病。氨基葡萄糖(GLC)是一种氨基单糖,在人类和动物软骨的合成过程中发挥着非常重要的作用。葡萄糖胺常用于治疗轻中度骨关节炎,具有良好的抗炎和抗氧化作用。本研究在小鼠和人类正常肝细胞 L02 细胞中构建了酒精损伤模型,以探讨 GLC 对 ALD 的保护作用和机制。给小鼠灌胃 GLC 30 天。小鼠和 L02 细胞的肝损伤模型均由乙醇产生。通过不同的试剂盒检测肝损伤生物标志物、脂代谢、氧化应激生物标志物和炎症因子的水平。通过 Western 印迹和 RT-PCR 探索小鼠肝组织中的氧化和炎症通路。结果表明,GLC 能明显抑制天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)的异常升高、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),并能显著改善高密度脂蛋白胆固醇(HDL-C)的水平。此外,通过降低肝脏中丙二醛(MDA)的水平,提高谷胱甘肽(GSH)、过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的水平,GLC 的干预能明显改善酒精引起的肝脏氧化应激。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,激活抗氧化通路 Keap1/Nrf2/HO-1,下调 MAPK 和 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 可能是减轻酒精引起的急性肝损伤的重要候选功能食品。
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来源期刊
Current Research in Food Science
Current Research in Food Science Agricultural and Biological Sciences-Food Science
CiteScore
7.40
自引率
3.20%
发文量
232
审稿时长
84 days
期刊介绍: Current Research in Food Science is an international peer-reviewed journal dedicated to advancing the breadth of knowledge in the field of food science. It serves as a platform for publishing original research articles and short communications that encompass a wide array of topics, including food chemistry, physics, microbiology, nutrition, nutraceuticals, process and package engineering, materials science, food sustainability, and food security. By covering these diverse areas, the journal aims to provide a comprehensive source of the latest scientific findings and technological advancements that are shaping the future of the food industry. The journal's scope is designed to address the multidisciplinary nature of food science, reflecting its commitment to promoting innovation and ensuring the safety and quality of the food supply.
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