Salidroside downregulates microRNA‑133a and inhibits endothelial cell apoptosis induced by oxidized low‑density lipoprotein.

Abstract

Vascular endothelial cell apoptosis is regulated by microRNA-133a (miR-133a), which participates in the formation of atherosclerotic (AS) plaques, leading to the development of several cardiovascular diseases. Salidroside (SAL), the main component of Rhodiola, is considered to exert anti-AS effect; however, its mode of action remains unclear. Thus, the present study aimed to determine whether SAL inhibits endothelial cell apoptosis through the miR-133a pathway. Cultured human coronary artery endothelial cells (HCAECs) were exposed to oxidized low-density lipoprotein (ox-LDL). Cell viability and cytotoxicity were monitored by MTT assay. In parallel, the mRNA expression levels of miR-133a and Bcl-xL, and the protein levels of anti-apoptotic Bcl-xL and activated caspase-3 were measured. The apoptotic levels were examined by flow cytometry. Furthermore, the effects of silencing and overexpressing miR-133a on the parameters mentioned above were evaluated. Exposure to ox-LDL induced an increase in the expression of miR-133a, with a concomitant decrease in the level of Bcl-xL in the HCAECs; these effects were reversed by treatment with SAL. Importantly, the effects of SAL were impaired upon the silencing of miR-133a, whereas the overexpression of miR-133a partly restored the effects of SAL. On the whole, the findings of the present study demonstrate that SAL inhibits the ox-LDL-induced upregulation of miR-133a expression, while promoting the expression of Bcl-xL, thereby preventing endothelial cell apoptosis.