Wang Lei, Li Aoyun, Zhang Xiaohu, Iqbal Mudassar, Aabdin Zain Ul, Xu Mengen, Mo Quan, Li Jiakui
College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.
College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, China.
Front Microbiol. 2025 Mar 5;16:1550556. doi: 10.3389/fmicb.2025.1550556. eCollection 2025.
Acute hepatic injury is a severe condition that is always accompanied by oxidative stress and inflammation, seriously threatening the health of the host. Probiotics have been shown to be involved in the regulation of antioxidant system and gut microbiota activity, but studies on the effects of yak derived () on acute liver injury and oxidative stress remain scarce. Here, we aim to explore the ameliorative effects of isolated from yaks on oxidative stress and hepatic injury caused by D-galactose, as well as the underlying processes. Results indicated that administration, particularly the BS3, significantly mitigated hepatic damage induced by D-galactose in mice as evidenced by ameliorating liver tissue damage as well as decreasing ALT ( < 0.05) and AST ( < 0.05) levels. Additionally, the intervention was demonstrated to enhance the antioxidant system in D-galactose-exposed mice, as manifested by increased T-AOC and SOD, alongside a decrease in MDA levels ( < 0.05). Meanwhile, intervention could effectively mitigate oxidative damage via modulating the Keap1/Nrf2 signaling pathway. Importantly, exhibited a pronounced protective effect against D-galactose-induced intestinal barrier dysfunction through improving tight junction proteins. The gut microbiota results suggest that BS3 alters the abundance of some gut flora such as Firmicutes phylum and and genera, which affects the composition of the gut microbiota and reverses the decrease in the microbial richness index in mice. In summary, these findings demonstrated that isolated from yaks serve as a promising candidate to ameliorate oxidative damage and hepatic injury. Meanwhile, the positive regulation effect of on gut microbiota and intestinal mucosal barrier may be one of its underlying mechanisms to alleviate oxidative stress and hepatic injury.
急性肝损伤是一种严重病症，常伴有氧化应激和炎症，严重威胁宿主健康。益生菌已被证明参与抗氧化系统和肠道微生物群活性的调节，但关于牦牛源（）对急性肝损伤和氧化应激影响的研究仍然很少。在此，我们旨在探讨从牦牛中分离出的（）对D-半乳糖引起的氧化应激和肝损伤的改善作用及其潜在机制。结果表明，给予（），特别是BS3，可显著减轻D-半乳糖诱导的小鼠肝损伤，这通过改善肝组织损伤以及降低ALT（<0.05）和AST（<0.05）水平得以证明。此外，（）干预可增强D-半乳糖处理小鼠的抗氧化系统，表现为T-AOC和SOD增加，同时MDA水平降低（<0.05）。同时，（）干预可通过调节Keap1/Nrf2信号通路有效减轻氧化损伤。重要的是，（）通过改善紧密连接蛋白对D-半乳糖诱导的肠道屏障功能障碍具有显著的保护作用。肠道微生物群结果表明，BS3改变了一些肠道菌群的丰度，如厚壁菌门以及（）和（）属，这影响了肠道微生物群的组成，并逆转了小鼠微生物丰富度指数的下降。总之，这些发现表明，从牦牛中分离出的（）有望改善氧化损伤和肝损伤。同时，（）对肠道微生物群和肠黏膜屏障的正向调节作用可能是其减轻氧化应激和肝损伤的潜在机制之一。
