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齐墩果酸通过 PI3K/Akt 信号通路缓解肥胖诱导的骨骼肌萎缩。

Oleanolic acid alleviates obesity-induced skeletal muscle atrophy via the PI3K/Akt signaling pathway.

机构信息

College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.

出版信息

FEBS Open Bio. 2024 Apr;14(4):584-597. doi: 10.1002/2211-5463.13780. Epub 2024 Feb 17.

DOI:10.1002/2211-5463.13780
PMID:38366735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10988678/
Abstract

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.

摘要

齐墩果酸（OA）是一种五环三萜，据报道具有预防多种疾病的作用，包括糖尿病、肝炎和各种癌症。然而，OA 对肥胖引起的肌肉萎缩的影响在很大程度上尚不清楚。本研究探讨了 OA 对 C2C12 细胞骨骼肌生成和增殖的影响。我们报告说，OA 可显著增加骨骼肌质量，并改善葡萄糖不耐受和胰岛素抵抗。OA 通过调节 PI3K/Akt 信号通路抑制地塞米松（Dex）诱导的 C2C12 成肌细胞萎缩。此外，它还抑制了肥胖小鼠肌肉萎缩时肌肉中 MuRF1 和 Atrogin1 基因的表达，增加了 PI3K 和 Akt 的激活，从而促进蛋白质合成，最终缓解肌肉萎缩。综上所述，这些发现表明 OA 可能具有预防和治疗肌肉萎缩的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/2803953abae9/FEB4-14-584-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/854030a592c2/FEB4-14-584-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/809e9baa50d8/FEB4-14-584-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/afbc378c5b73/FEB4-14-584-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/bff1e3ea8c75/FEB4-14-584-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/2803953abae9/FEB4-14-584-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/854030a592c2/FEB4-14-584-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/809e9baa50d8/FEB4-14-584-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/afbc378c5b73/FEB4-14-584-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/bff1e3ea8c75/FEB4-14-584-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95ac/10988678/2803953abae9/FEB4-14-584-g005.jpg

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