Zhang Yuhang, Yang Ge, Gao Yansong, Gao Lei, Kang You, Zhao Yujuan, Zhao Lei, Li Shengyu
School of Pharmaceutical Sciences, Changchun University of Chinese Medicine, Changchun 130117, PR China.
Institute of Agro-food Technology, Jilin Academy of Agricultural Sciences (Northeast Agricultural Research Center of China), Changchun 130033, PR China.
Life Sci. 2024 Dec 15;359:123231. doi: 10.1016/j.lfs.2024.123231. Epub 2024 Nov 12.
Minor ginsenosides have demonstrated notable anti-fatigue capabilities. The aim of this study was to investigate the anti-fatigue mechanisms of total minor ginsenosides (TMGs) derived from a process involving probiotic fermentation and high-pressure steam treatment. The fatigue model was established in BALB/c male mice using weight-bearing swimming and TMGs were administered by orally at a dosage of 200 mg/kg for four weeks. The anti-fatigue mechanisms of TMGs were explored by assessing liver oxidative stress, skeletal muscle inflammation markers, as well as their impact on gut microbiota and serum metabolism. The results indicated that TMGs could significantly increase the levels of SOD, CAT, ATP and Na-K-ATPase and enhance the antioxidant capacity by modulating the PGC-1α/KEAP1/NRF2/HO-1 pathway. Meanwhile, TMGs reducing the levels of inflammatory factors TNF-α, IL-1β and IL-6 and inhibited inflammation by modulating the AMPK/TORC2/CREB/PGC-1α pathway. TMGs also regulated the gut microbiota, increasing the abundance of probiotic bacteria and the content of short-chain fatty acids (SCFAs) in the cecum. Serum metabolomics analyses have shown that TMGs can significantly affect the serum metabolic profile of fatigue model mice, regulating metabolic markers through affecting anti-fatigue-related metabolic pathways. In conclusion, TMGs exerted significant anti-fatigue effects through antioxidant and anti-inflammatory effects, and alleviate fatigue by regulating gut microbiota and serum metabolism.
小分子人参皂苷已显示出显著的抗疲劳能力。本研究的目的是探讨经益生菌发酵和高压蒸汽处理过程得到的总小分子人参皂苷（TMGs）的抗疲劳机制。采用负重游泳法在BALB/c雄性小鼠中建立疲劳模型，并以200 mg/kg的剂量口服给予TMGs，持续四周。通过评估肝脏氧化应激、骨骼肌炎症标志物以及它们对肠道微生物群和血清代谢的影响，来探究TMGs的抗疲劳机制。结果表明，TMGs可显著提高超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、三磷酸腺苷（ATP）和钠钾ATP酶的水平，并通过调节PGC-1α/KEAP1/NRF2/HO-1信号通路增强抗氧化能力。同时，TMGs降低炎症因子肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的水平，并通过调节AMPK/TORC2/CREB/PGC-1α信号通路抑制炎症。TMGs还调节肠道微生物群，增加益生菌的丰度和盲肠中短链脂肪酸（SCFAs）的含量。血清代谢组学分析表明，TMGs可显著影响疲劳模型小鼠的血清代谢谱，通过影响抗疲劳相关代谢途径调节代谢标志物。总之，TMGs通过抗氧化和抗炎作用发挥显著的抗疲劳效果，并通过调节肠道微生物群和血清代谢来缓解疲劳。
