Geng Xiong, Zhuang Miaomiao, Tian Weina, Shang Huayan, Gong Ziyi, Lv Yanfang, Li Jianrong
College of Food Science and Engineering, Bohai University, Jinzhou 121013, China.
Foods. 2024 Nov 22;13(23):3733. doi: 10.3390/foods13233733.
This study aimed to ascertain the potential benefits of green radish polysaccharide (GRP) in treating alcoholic liver disease (ALD) in mice and explore its mechanism of action. Using biochemical analysis, high-throughput sequencing of gut microbiota, and gas chromatography-mass spectrometry to measure short-chain fatty acids (SCFAs) in feces, we found that GRP intervention significantly improved lipid metabolism and hepatic function in mice subjected to excessive alcohol intake. The GRP intervention reduced malondialdehyde levels by 66% and increased total superoxide dismutase levels by 22%, thereby mitigating alcohol-induced oxidative stress. Furthermore, GRP intervention in mice with alcohol consumption resulted in a reduction in tumor necrosis factor, interleukin 6, and lipopolysaccharide levels by 12%, 9%, and 25%, respectively, effectively attenuating alcoholic liver inflammation. 16S rRNA amplicon sequencing demonstrated that excessive alcohol consumption markedly altered the gut microbiota composition in mice. The GRP treatment resulted in a significant reduction in the number of beneficial bacteria ( and ) and an increase in the proportion of harmful bacteria ( and ). The metabolomic analyses of the SCFAs demonstrated an increase in the contents of SCFAs, acetic acid, propionic acid, and butyric acid, following GRP supplementation. Furthermore, the metabolic levels of cholinergic synapses and glycolysis/gluconeogenesis were found to be modulated. In conclusion, these findings suggest that GRP may attenuate alcohol-induced oxidative damage in the liver by modulating the gut microbiota and hepatic metabolic pathways. This may position GRP as a potential functional component for ALD prevention.
本研究旨在确定绿萝多糖(GRP)对治疗小鼠酒精性肝病(ALD)的潜在益处,并探索其作用机制。通过生化分析、肠道微生物群高通量测序以及气相色谱-质谱联用技术测定粪便中的短链脂肪酸(SCFA),我们发现GRP干预显著改善了过量饮酒小鼠的脂质代谢和肝功能。GRP干预使丙二醛水平降低了66%,总超氧化物歧化酶水平提高了22%,从而减轻了酒精诱导的氧化应激。此外,对饮酒小鼠进行GRP干预后,肿瘤坏死因子、白细胞介素6和脂多糖水平分别降低了12%、9%和25%,有效减轻了酒精性肝脏炎症。16S rRNA扩增子测序表明,过量饮酒显著改变了小鼠的肠道微生物群组成。GRP治疗导致有益菌(和)数量显著减少,有害菌(和)比例增加。对SCFA的代谢组学分析表明,补充GRP后SCFA、乙酸、丙酸和丁酸的含量增加。此外,还发现胆碱能突触和糖酵解/糖异生的代谢水平受到调节。总之,这些发现表明,GRP可能通过调节肠道微生物群和肝脏代谢途径减轻酒精诱导的肝脏氧化损伤。这可能使GRP成为预防ALD的潜在功能成分。