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| 补肾强筋胶囊改善肌少症机制研究 |
| The mechanism of action of the Nourishing Kidney and Strengthening Tendon Capsule in the treatment of sarcopenia through PI3K/AKT/FoxO3α pathway |
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| DOI：10.3969/j.issn.1006-7108.2026.05.005 |
| 中文关键词: 补肾强筋胶囊 C2C12成肌细胞 肌少症 PI3K/AKT/FoxO3α信号通路 肌萎缩 |
| 英文关键词:the Nourishing Kidney and Strengthening Tendon Capsule C2C12 myoblasts sarcopenia PI3K/AKT/FoxO3α signaling pathway muscle atrophy |
| 基金项目:广州市科技局重点研发计划项目(202206010048)；“广东特支计划”省卫生健康委领军人才项目[粤卫人函(2024)54号]；广州地区中西医协同临床重大创新技术建设项目[穗卫函(2023)2318号]；广州市科技局基础与应用基础研究项目（202201011291） |
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| 中文摘要: |
| 目的 探究补肾强筋胶囊对地塞米松诱导的C2C12成肌细胞萎缩及肌萎缩大鼠的保护作用。方法 利用网络药理学预测补肾强筋胶囊治疗肌少症的潜在作用靶点，开展PPI互作分析，并借助Metascape进行富集分析以明确相关通路。在体外实验中，构建地塞米松诱导的C2C12成肌细胞萎缩模型，以不同浓度的补肾强筋胶囊含药血清进行干预，通过CCK-8法确定最佳药物浓度，并观察细胞分化状态、计算肌管直径，同时采用Western blot检测肌肉生成标志物MyoD1和肌肉萎缩标志物Atrogin-1的表达以及PI3K/AKT/FoxO3α信号通路蛋白表达。在体内实验中，构建肌萎缩大鼠模型，经补肾强筋胶囊干预后，利用HE染色、WGA染色和免疫组化等方法评估其治疗作用。结果 网络药理学研究提示补肾强筋胶囊可能通过PI3K/AKT/FoxO3α信号通路改善肌少症。体外实验中，2.5 %浓度的含药血清对C2C12成肌细胞活力最佳，可缓解肌细胞萎缩，改善地塞米松抑制的MyoD1表达，降低升高的Atrogin-1水平，且能提高PI3K、Akt磷酸化水平。体内实验表明，补肾强筋胶囊可治疗股四头肌萎缩，促进肌内MyoD-1蛋白表达，抑制肌萎缩蛋白Atrogin-1表达。结论 补肾强筋胶囊能够通过调节PI3K/AKT/FoxO3α信号通路改善肌肉萎缩。 |
| 英文摘要: |
| Objective This study aimed to explore the protective effects of the Nourishing Kidney and Strengthening Tendon Capsule Capsule on dexamethasone-induced C2C12 myoblast atrophy and muscle-atrophied rats. Methods Network pharmacology was used to predict the potential targets of the Nourishing Kidney and Strengthening Tendon Capsule Capsule for the sarcopenia treatment. PPI interaction analysis was conducted. Metascape was employed for enrichment analysis to identify the related pathways. A dexamethasone-induced C2C12 myoblast atrophy model was established in vitro. Different concentrations of the Nourishing Kidney and Strengthening Tendon Capsule Capsule-containing serum were used for intervention. The optimal drug concentration was determined with CCK-8 assay. Cell differentiation status and myotube diameter were observed. Western blotting was used to detect the expression of the muscle generation marker MyoD1, muscle atrophy marker Atrogin 1, and proteins in the PI3K/AKT/FoxO3α signaling pathway. A muscle-atrophied rat model was established in vivo. After intervention with the Nourishing Kidney and Strengthening Tendon Capsule Capsule, therapeutic effects were assessed using HE staining, WGA staining, and immunohistochemistry. Results Network pharmacology suggested that the Nourishing Kidney and Strengthening Tendon Capsule Capsule might relieve sarcopenia via the PI3K/AKT/FoxO3α signaling pathway. In vitro, the best vitality for C2C12 myoblasts was showed with addition of 2.5% drug-containing serum. Under this condition, myocyte atrophy was alleviated, MyoD1 expression suppressed by dexamethasone was improved, elevated Atrogin 1 levels was reduced, and the PI3K and Akt phosphorylation levels increased. In vivo experiments indicated that the Nourishing Kidney and Strengthening Tendon Capsule Capsule could treat quadriceps atrophy, promote MyoD protein expression in muscles, and inhibit Atrogin 1 expression. Conclusion the Nourishing Kidney and Strengthening Tendon Capsule relieve the muscle atrophy by modulating the PI3K/AKT/FoxO3α signaling pathway. |
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