Oleanolic acid (OA) is a pentacyclic triterpene with reported protective effects against various diseases, including diabetes, hepatitis, and different cancers. However, the effects of OA on obesity-induced muscle atrophy remain largely unknown. This study investigated the effects of OA on skeletal muscle production and proliferation of C2C12 cells. We report that OA significantly increased skeletal muscle mass and improved glucose intolerance and insulin resistance. OA inhibited dexamethasone (Dex)-induced muscle atrophy in C2C12 myoblasts by regulating the PI3K/Akt signaling pathway. In addition, it also inhibited expression of MuRF1 and Atrogin1 genes in skeletal muscle of obese mice suffering from muscle atrophy, and increased the activation of PI3K and Akt, thereby promoting protein synthesis, and eventually alleviating muscle atrophy. Taken together, these findings suggest OA may have potential for the prevention and treatment of muscle atrophy.

中文翻译：

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齐墩果酸通过 PI3K/Akt 信号通路减轻肥胖引起的骨骼肌萎缩

齐墩果酸 (OA) 是一种五环三萜，据报道对多种疾病具有保护作用，包括糖尿病、肝炎和不同的癌症。然而，OA 对肥胖引起的肌肉萎缩的影响仍然很大程度上未知。本研究调查了 OA 对骨骼肌生成和 C2C12 细胞增殖的影响。我们报告说，OA 显着增加了骨骼肌质量并改善了葡萄糖耐受不良和胰岛素抵抗。 OA 通过调节 PI3K/Akt 信号通路抑制地塞米松 (Dex) 诱导的 C2C12 成肌细胞肌肉萎缩。此外，它还能抑制患有肌肉萎缩的肥胖小鼠骨骼肌中MuRF1和Atrogin1基因的表达，并增加PI3K和Akt的激活，从而促进蛋白质合成，最终缓解肌肉萎缩。总而言之，这些发现表明 OA 可能具有预防和治疗肌肉萎缩的潜力。