OBJECTIVES: Emerging evidence showed that muscone could improve chronic inflammation after myocardial infarction and protect alcohol-induced osteonecrosis of the femoral head. However, the function of muscone on diabetic peripheral neuropathy (DPN) is obscure. METHODS: The neuronal Schwann cell RSC 96 cells were treated with 125 mmol/l glucose to simulate the cells in DPN. The RSC 96 cell viability was detected by cell counting kit-8. The RSC 96 cell cycle and apoptosis were determined by flow cytometry. The expression of marker proteins of apoptosis, autophagy and AKT/mTOR signalling pathway was assessed by Western blot. KEY FINDINGS: We observed that after high glucose (HG) treatment, the number of cell apoptosis was increased, cell proliferation was decreased, as well as the expression of apoptosis-related proteins and autophagy-related proteins were changed. However, this phenomenon can be reversed by muscone. Meanwhile, the expression of phosphorylated AKT and mammalian target of rapamycin (mTOR) was down-regulated with HG treatment, while the expression quantity was up-regulated after disposed with muscone. CONCLUSIONS: Our outcomes demonstrated that autophagy and apoptosis of RSC 96 cells induced by HG can be alleviated by muscone through modulating AKT/mTOR signalling pathway, suggesting that muscone might be a potential molecule with influence in connection to DPN.
