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

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.