Cao Ying-Jia, Huang Zi-Rui, You Shi-Ze, Guo Wei-Ling, Zhang Fang, Liu Bin, Lv Xu-Cong, Lin Zhan-Xi, Liu Peng-Hu
National Engineering Research Center of JUNCAO Technology, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Institute of Food Science and Technology, College of Biological Science and Technology, Fuzhou University, Fuzhou 350108, China.
Foods. 2022 Mar 25;11(7):949. doi: 10.3390/foods11070949.
This study aimed to investigate the protective effects of ganoderic acids (GA) from against liver injury and intestinal microbial disorder in mice with excessive alcohol intake. Results showed GA supplement significantly inhibited the abnormal elevation of the liver index, serum lipid parameters, aspartate aminotransferase and alanine aminotransferase in mice exposed to alcohol intake, and also significantly protected the excessive lipid accumulation and pathological changes. Alcohol-induced oxidative stress in the liver was significantly ameliorated by GA intervention through reducing the levels of maleic dialdehyde and lactate dehydrogenase and increasing the levels of glutathione, catalase, superoxide dismutase and alcohol dehydrogenase. Intestinal microbiota profiling demonstrated GA intervention modulated the composition of intestinal microflora by increasing the levels of , , , and decreasing the level. Furthermore, liver metabolomic profiling suggested GA intervention had a remarkable regulatory effect on liver metabolism with excessive alcohol consumption. Moreover, GA intervention regulated mRNA levels of alcohol metabolism, fatty lipid metabolism, oxidative stress, bile acid biosynthesis and metabolism-related genes in the liver. Conclusively, these findings demonstrate GA intervention can significantly relieve alcoholic liver injury and it is hopeful to become a new functional food ingredient for the prevention of alcoholic liver injury.
本研究旨在探讨灵芝酸(GA)对过量饮酒小鼠肝损伤和肠道微生物紊乱的保护作用。结果显示,补充GA可显著抑制饮酒小鼠肝脏指数、血脂参数、天冬氨酸转氨酶和丙氨酸转氨酶的异常升高,还能显著保护肝脏过度的脂质蓄积和病理变化。GA干预通过降低丙二醛和乳酸脱氢酶水平,提高谷胱甘肽、过氧化氢酶、超氧化物歧化酶和乙醇脱氢酶水平,显著改善了酒精诱导的肝脏氧化应激。肠道微生物群分析表明,GA干预通过提高[具体微生物名称1]、[具体微生物名称2]、[具体微生物名称3]、[具体微生物名称4]水平和降低[具体微生物名称5]水平来调节肠道微生物群的组成。此外,肝脏代谢组分析表明,GA干预对过量饮酒时的肝脏代谢具有显著的调节作用。此外,GA干预调节了肝脏中酒精代谢、脂质代谢、氧化应激、胆汁酸生物合成和代谢相关基因的mRNA水平。总之,这些发现表明GA干预可显著减轻酒精性肝损伤,有望成为预防酒精性肝损伤的新型功能性食品成分。