向青, 李钻芳, 胡悦, 陈聪, 刘志臻, 陶静, 陈立典. 基于腓肠肌代谢组学研究山芋丸改善肌少症小鼠骨骼肌质量及运动功能的作用机制J. 药学学报, 2026, 61(1): 233-243. DOI: 10.16438/j.0513-4870.2025-0858
引用本文: 向青, 李钻芳, 胡悦, 陈聪, 刘志臻, 陶静, 陈立典. 基于腓肠肌代谢组学研究山芋丸改善肌少症小鼠骨骼肌质量及运动功能的作用机制J. 药学学报, 2026, 61(1): 233-243. DOI: 10.16438/j.0513-4870.2025-0858
XIANG Qing, LI Zuan-fang, HU Yue, CHEN Cong, LIU Zhi-zhen, TAO Jing, CHEN Li-dian. Study on effect mechanism of Shanyu Pills in improving skeletal muscle mass and motor function in sarcopenia mice based on gastrocnemius muscle metabolomicsJ. Acta Pharmaceutica Sinica, 2026, 61(1): 233-243. DOI: 10.16438/j.0513-4870.2025-0858
Citation: XIANG Qing, LI Zuan-fang, HU Yue, CHEN Cong, LIU Zhi-zhen, TAO Jing, CHEN Li-dian. Study on effect mechanism of Shanyu Pills in improving skeletal muscle mass and motor function in sarcopenia mice based on gastrocnemius muscle metabolomicsJ. Acta Pharmaceutica Sinica, 2026, 61(1): 233-243. DOI: 10.16438/j.0513-4870.2025-0858

基于腓肠肌代谢组学研究山芋丸改善肌少症小鼠骨骼肌质量及运动功能的作用机制

Study on effect mechanism of Shanyu Pills in improving skeletal muscle mass and motor function in sarcopenia mice based on gastrocnemius muscle metabolomics

  • 摘要: 本研究通过评价山芋丸(Shanyu Pills)对肌少症小鼠骨骼肌质量、运动功能及腓肠肌代谢物的影响, 探究山芋丸治疗肌少症的科学内涵。所有动物实验经福建中医药大学实验动物伦理委员会批准(批准号: FJTCM IACUC 2022123)。采用8月龄快速老化小鼠SAMP8 (senescence accelerated mouse prone/8, SAMP8)作为肌少症小鼠动物模型, 通过检测小鼠衰老分级评分、后肢肌肉体积、抓力、疲劳转棒停留时间、抓网悬挂时长、自由活动度、脾虚生化指标及腓肠肌组织病理学, 评价山芋丸改善肌少症小鼠骨骼肌质量及运动功能的生物效应。运用LC-MS/MS技术对小鼠腓肠肌代谢物进行分析, 通过正交偏最小二乘法判别分析(OPLS-DA) 筛选出各比较组间差异代谢物, 并利用MetaboAnalyst 6.0数据库对差异代谢物进行代谢通路富集分析、Cytoscape 3.10.0软件构建差异代谢物的“Compound-Reaction-Enzyme-Gene”网络。结果表明, 山芋丸能显著降低肌少症小鼠衰老分级评分; 增加肌少症小鼠后肢肌肉体积、抓力、疲劳转棒停留时间、抓网悬挂时长、自由活动度; 改善脾虚生化指标和腓肠肌肌纤维萎缩现象。腓肠肌非靶向代谢组学分析结果显示, 山芋丸主要影响了花生四烯酸、白三烯、肌肽、甲基咪唑乙酸等14个差异代谢物, 富集得到的潜在靶点代谢通路为花生四烯酸代谢通路。综上, 山芋丸能有效改善肌少症小鼠骨骼肌质量和运动功能, 其机制可能与调控花生四烯酸代谢密切相关。

     

    Abstract: This study evaluated the effects of Shanyu Pills on the skeletal muscle mass, motor function, and metabolites of the gastrocnemius muscle in sarcopenia mice, aiming to explore the scientific essence of Shanyu Pills in treating sarcopenia. All animal experiments were approved by the Experimental Animal Ethics Committee of Fujian University of Traditional Chinese Medicine (approval No.: FJTCM IACUC 2022123). Eight-month-old rapidly aging mice SAMP8 (senescence accelerated mouse prone/8, SAMP8) were used as the animal model for sarcopenia. The biological effects of Shanyu Pills in improving the skeletal muscle mass and motor function of mice with sarcopenia were evaluated by evaluating of the degree of senescence of mice, muscle volume of the hindlimbs, grip strength, hanging net duration time, rotarod performance time, free movement assessment, biochemical indicators of spleen deficiency, and histopathology of gastrocnemius muscle tissue. The metabolites in the gastrocnemius muscle of mice were analyzed using LC-MS/MS. Orthogonal Partial Least Squares Discriminant Analysis (OPLS-DA) was used to screen out the differential metabolites among different comparison groups. The differential metabolites were analyzed for metabolic pathway enrichment using the MetaboAnalyst 6.0 database and the "Compound-Reaction-Enzyme-Gene" network of the differential metabolites was constructed using Cytoscape 3.10.0 software. The results showed that Shanyu Pills could significantly reduce the degree of senescence of sarcopenia mice; increase the muscle volume of the hindlimbs, grip strength, hanging net duration time, rotarod performance time, free movement assessment; improve the biochemical indicators of spleen deficiency; and alleviate the phenomenon of gastrocnemius muscle fiber atrophy. The non-targeted metabolomics analysis of the gastrocnemius muscle showed that Shanyu Pills mainly affected 14 differential metabolites such as arachidonic acid, leukotriene A4, carnosine, methylimidazoleacetic acid. The potential target metabolic pathways enriched were the arachidonic acid metabolic pathway. In summary, Shanyu Pills can effectively improve the skeletal muscle mass and motor function of sarcopenia mice, and its mechanism may be closely related to the regulation of arachidonic acid metabolism.

     

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