Abstract
Salidroside, a major active ingredient isolated from Rhodiola rosea, has a long application in Chinese medical history. It has widely demonstrated effects on fatigue, psychological stress, and depression and exhibits potential antihypoxia activity. Emerging evidence shows that hypoxia is an important independent risk factor for erectile dysfunction (ED). The aim of this study was to clarify the effect of salidroside on hypoxia-induced phenotypic transformation of corpus cavernosum smooth muscle cells (CCSMCs). Our results showed that salidroside decreased the hypoxia-induced expression of collagen and content of vimentin, a corpus cavernosum smooth muscle synthetic protein, in vitro. Simultaneously, salidroside increased expression of the CCSMC contractile proteins, α-smooth muscle actin (α-SMA) and desmin. In vivo, similarly, the expressions of collagen and hypoxia-inducible factor-1α were increased in bilateral cavernous neurectomy (BCN) rats while they were decreased in the salidroside group. Among the phenotypic proteins, α-SMA and desmin increased and vimentin decreased after treating BCN rats with salidroside compared with the BCN alone group. Overall, our results demonstrate that salidroside has the ability to oppose hypoxia and can inhibit the CCSMC phenotypic transformation induced by hypoxia. Salidroside may provide a new treatment method for ED.
Highlights
Erectile dysfunction (ED) is considered a common clinical disease where the penis cannot reach or maintain sufficient erection to obtain satisfied coitus
Salidroside, a major active ingredient isolated from Rhodiola rosea, has been long used as a traditional Chinese medicine
Different concentrations of salidroside were added into corpus cavernosum smooth muscle cells (CCSMCs) cultures under normoxic and hypoxic environments
Summary
Erectile dysfunction (ED) is considered a common clinical disease where the penis cannot reach or maintain sufficient erection to obtain satisfied coitus. The total response rate for PDE5-Is in patients is poor; approximately 30–40% of men with ED do not respond to PDE5-Is therapy [2, 3]. These treatment failures may result from many different causes such as insufficient dose, insufficient sexual stimulation time, or even hypogonadism [4]. The target pathway of PDE5-Is is disturbed under the condition of cavernous nerve injury [5] and it is important to identify a more effective drug and provide new clinical treatment methods
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