Sexual medicine reviews · 2026
Molecular mechanisms of icariin in the treatment of erectile dysfunction.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Meng Chunyang, Jiang Rui
Аннотация
INTRODUCTION: The molecular mechanisms underlying the effects of icariin (ICA) on erectile dysfunction (ED) remain incompletely understood.
OBJECTIVE: To investigate the pharmacokinetics of ICA and its molecular mechanisms in the treatment of ED.
METHODS: A literature search was conducted in PubMed and Web of Science to identify studies evaluating the effects of ICA on erectile function.
RESULTS: The principal bioactive form of icariside in vivo is icariside II. ICA has been shown to improve under different pathological conditions through multiple molecular mechanisms, including activation of the NOS/NO/cGMP pathway, inhibition of the RhoA/ROCK pathway, reduction of autophagy in corpus cavernosum cells, suppression of advanced glycation end products, inhibition of programmed cell death in corpus cavernosum cells, inhibition of PDE5 activity, promotion of testosterone synthesis, and modulation of endogenous stem cell-related markers, which may contribute to penile tissue repair.
CONCLUSION: ICA may ameliorate pathological changes associated with ED animal models with different etiologies through multi-target mechanisms; however, its clinical efficacy still requires further confirmation in high-quality randomized controlled trials.
OBJECTIVE: To investigate the pharmacokinetics of ICA and its molecular mechanisms in the treatment of ED.
METHODS: A literature search was conducted in PubMed and Web of Science to identify studies evaluating the effects of ICA on erectile function.
RESULTS: The principal bioactive form of icariside in vivo is icariside II. ICA has been shown to improve under different pathological conditions through multiple molecular mechanisms, including activation of the NOS/NO/cGMP pathway, inhibition of the RhoA/ROCK pathway, reduction of autophagy in corpus cavernosum cells, suppression of advanced glycation end products, inhibition of programmed cell death in corpus cavernosum cells, inhibition of PDE5 activity, promotion of testosterone synthesis, and modulation of endogenous stem cell-related markers, which may contribute to penile tissue repair.
CONCLUSION: ICA may ameliorate pathological changes associated with ED animal models with different etiologies through multi-target mechanisms; however, its clinical efficacy still requires further confirmation in high-quality randomized controlled trials.