Guo Wei-Ling, Cao Ying-Jia, You Shi-Ze, Wu Qi, Zhang Fang, Han Jin-Zhi, Lv Xu-Cong, Rao Ping-Fan, Ai Lian-Zhong, Ni Li
Institute of Food Science and Technology, College of Biological Science and Technology, Fuzhou University, Fuzhou, Fujian, 350108, China.
School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, 214122, China.
Curr Res Food Sci. 2022 Feb 24;5:515-530. doi: 10.1016/j.crfs.2022.02.013. eCollection 2022.
Alcoholic liver injury is mainly caused by excessive alcohol consumption and has become a global public health problem threatening human health. It is well known that possesses various excellent beneficial effects on liver function and lipid metabolism. The purpose of this study was to evaluate the underlying protective effect and action mechanism of ganoderic acids-rich ethanol extract (GLE) on alcohol-induced liver injury in mice with excessive alcohol intake. Results showed that oral administration of GLE could obviously inhibit the abnormal increases of serum triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and also significantly protect the liver against alcohol-induced excessive hepatic lipid accumulation and pathological changes. In addition, alcohol-induced oxidative stress in liver was significantly ameliorated by the dietary intervention of GLE through reducing the hepatic levels of maleic dialdehyde (MDA) and lactate dehydrogenase (LDH), and increasing the hepatic levels of glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and alcohol dehydrogenase (ADH). Compared with the model group, GLE intervention significantly ameliorated the intestinal microbial disorder by elevating the relative abundance of _9, _UCG-001, , group, norank_f_Clostridiates_vadinBB60_group, GCA-900066225, , UCG-009, norank_f and , but decreasing the proportion of _sensu__1. Furthermore, liver metabolomic profiling suggested that GLE intervention had a significant regulatory effect on the composition of liver metabolites in mice with excessive alcohol intake, especially the levels of some biomarkers involved in primary bile acid biosynthesis, riboflavin metabolism, tryptophan metabolism, biosynthesis of unsaturated fatty acids, fructose and mannose metabolism, glycolysis/gluconeogenesis. Additionally, dietary supplementation with GLE significantly regulated the mRNA levels of key genes related to fatty acids metabolism, ethanol catabolism and inflammatory response in liver. Conclusively, these findings indicate that GLE has a potentially beneficial effect on alleviating alcohol-induced liver injury and may be developed as a promising functional food ingredient.
酒精性肝损伤主要由过量饮酒引起，已成为威胁人类健康的全球性公共卫生问题。众所周知，其对肝功能和脂质代谢具有多种优异的有益作用。本研究的目的是评估富含灵芝酸的乙醇提取物（GLE）对过量饮酒小鼠酒精性肝损伤的潜在保护作用及作用机制。结果表明，口服GLE可明显抑制血清甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）的异常升高，还能显著保护肝脏免受酒精诱导的过度肝脂质蓄积和病理变化。此外，通过降低肝脏中丙二醛（MDA）和乳酸脱氢酶（LDH）水平，提高谷胱甘肽（GSH）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和乙醇脱氢酶（ADH）水平，GLE的饮食干预显著改善了酒精诱导的肝脏氧化应激。与模型组相比，GLE干预通过提高_9、_UCG - 001、、_组、norank_f_Clostridiates_vadinBB60_组、GCA - 900066225、、UCG - 009、norank_f_和的相对丰度，但降低_sensu__1的比例，显著改善了肠道微生物紊乱。此外，肝脏代谢组学分析表明，GLE干预对过量饮酒小鼠肝脏代谢物组成具有显著调节作用，尤其是对一些参与初级胆汁酸生物合成过程、核黄素代谢、色氨酸代谢、不饱和脂肪酸生物合成、果糖和甘露糖代谢、糖酵解/糖异生的生物标志物水平。此外，饮食中补充GLE显著调节了肝脏中与脂肪酸代谢、乙醇分解代谢和炎症反应相关关键基因的mRNA水平。总之，这些发现表明GLE对减轻酒精性肝损伤具有潜在有益作用，可能被开发成为一种有前景的功能性食品成分。
