Muscone ameliorates diabetic peripheral neuropathy through activating AKT/mTOR signalling pathway.

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.