PDF(Pubmed)
Abstract：
Using treadmill training, this study replicated human exercise conditions and triggered exercise-induced fatigue in mice to examine the potential of Pediococcus pentosaceus YF01 in delaying this fatigue by regulating oxidative stress and its impact on the exercise capacity and gut microbiota of mice. The exercise capacity of mice was tested by conducting exhaustion tests, determining histopathological changes in mouse tissues, detecting the levels of serum biochemical markers, and evaluating the mRNA expression levels of relevant genes. YF01 prolonged the exhaustion time of mice, increased the serum levels of oxidative stress-related markers T-AOC, CAT, and GSH, as well as GLU and LA levels in the mice. YF01 decreased the levels of hepatic-related markers AST and ALT, as well as exercise-related markers LDH, BUN, UA, and CRE in the mice. YF01 upregulated the mRNA expression of MyHc I, SIRT1, and PGC in muscle tissues, as well as SOD1, SOD2, and CAT in both liver and muscle tissues. YF01 also downregulated the mRNA expression of MyHc IIa, MyHc IIb, and MyHc IIx in muscle tissues. Furthermore, YF01 increased the abundance of beneficial bacteria such as Lactobacillus and Lachnospiraceae in the gut microbiota of mice. In conclusion, P. pentosaceus YF01 may affect the exercise capacity of mice by modulating oxidative stress levels, thereby offering novel ideas for developing of sports science and human health.
摘要：
使用跑步机训练，这项研究复制了人类的运动条件，并引发了小鼠的运动性疲劳，以研究戊糖片球菌YF01通过调节氧化应激及其对小鼠运动能力和肠道菌群的影响来延缓这种疲劳的潜力。通过进行力竭试验测试小鼠的运动能力,确定小鼠组织的组织病理学变化，检测血清生化标志物的水平，并评估相关基因的mRNA表达水平。YF01延长了小鼠的耗尽时间，血清氧化应激相关标志物T-AOC水平升高，CAT,GSH,以及小鼠中的GLU和LA水平。YF01降低了肝脏相关标志物AST和ALT的水平，以及与运动相关的标志物LDH，BUN,UA,和老鼠身上的CRE。YF01上调MyHcI的mRNA表达，SIRT1和PGC在肌肉组织中，以及肝脏和肌肉组织中的SOD1，SOD2和CAT。YF01还下调MyHcIIa的mRNA表达，MyHcIIb,和MyHcIIx在肌肉组织中。此外，YF01增加了小鼠肠道微生物群中有益细菌的丰度，例如乳酸菌和落叶松科。总之,PentosacusYF01可能通过调节氧化应激水平影响小鼠的运动能力，从而为体育科学和人类健康的发展提供了新的思路。
