In brief, the results of our present study indicate that salidroside, a major active ingredient isolated from Rhodiola rosea, can resist hypoxia and prevent hypoxia-induced CCSMC phenotypic transformation through antihypoxia activities.
Indeed, our previous study indicated that corpus cavernosum smooth muscle cells (CCSMCs) can shift from the contractile to synthetic phenotype under hypoxic conditions .
Nevertheless, the ability of salidroside to inhibit hypoxia-induced changes on CCSMCs remains unclear.
The aim of this study was to reveal the ability of salidroside to resist hypoxia and inhibit phenotype modulation of CCSMCs. Clarification of the effect of salidroside on phenotypic modulation caused by hypoxia might provide a new therapy for ED and have significant clinical value.
The expression of HIF-1[alpha] increased after exposure of CCSMCs to hypoxia.
According to our previous research and other reports [14-16], when hypoxia occurs in CCSMCs, [alpha]-SMA and desmin (contractile proteins of the CCSM) are downregulated, whereas vimentin (a smooth muscle synthetic marker protein) is significantly upregulated.
Furthermore, HIF-1[alpha] plays an important role in the phenotypic transformation process in CCSMCs. Similar to our previous results , we showed that the expression of collagen in the extracellular matrix and HIF-1[alpha] levels increased significantly in CCSMCs in response to hypoxia.
Salidroside decreased the expression of HIF-1[alpha] and retained the contractile properties of CCSMCs. At the same time, salidroside inhibited transformation of cavernous smooth muscle from the contractile to the synthetic state.