Slibinin governs high glucose induced autophagy in cardiac myocyte cells via sphingosine kinase 1 pathway

As a disorder of the myocardium caused by diabetes mellitus, DCM has become a key health concern in the Delivered by Ingenta world. Autophagy plays an important role in the pathogenesis of DCM. Sphingosine kinase 1 benefits to cell survival and growth, and regulates the pathogenesis of many diseases, including diabetes and cardiovascular disease. Silibinin is widely used as a hepatoprotective and antioxidant agent in Asia and Europe. However, how silibinin governs DCM remains poorly understood. To this aim, the present study is to mine the role of Sphk1 in autophagy induction and cell survival in myocardial cells under high glucose treatment, and how silibinin regulates DCM. Herein, the study used the embryonic rat heart-derived myogenic H9C2 cells and adenovirus based gene manipulation was utilized. It was found that silibinin could induce autophagy in a dose-dependent manner. Overexpression of Sphk1 significantly increased mRNA expression of autophagy gene markers in H9C2 cells. Gain of function of Sphk1 significantly increased protein level of Beclin1 in H9C2 cells under treatments of low (5.5 mM) and high (25 mM) glucose. High glucose inhibited autophagy induction in H9C2 cells. Gain of function of Sphk1 compromised inhibition of on autophagy induction by high glucose. The results of the present study may assist in attaining an improved understanding of the pathogenesis of DCM, and developing novel therapies for treatment of DCM.

Automated summary

This study explored the role of Sphk1 in autophagy induction and cell survival in myocardial cells under high glucose treatment, as well as how silibinin regulates DCM. The results showed that silibinin could induce autophagy in a dose-dependent manner, and overexpression of Sphk1 increased the expression of autophagy gene markers. High glucose inhibited autophagy induction, but overexpression of Sphk1 counteracted this inhibitory effect.