Publications by authors named "Miao-Yong Ye"

Objective: To verify the effect of Buyang Huanwu Decoction (BHD) in ameliorating erectile dysfunction (ED) after radical prostatectomy (RP).

Methods: The composition of BHD was verified by ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS/MS) analysis. Bilateral cavernous nerve crush injury (BCNI) in rats was used to mimic the neurovascular injury occurring after RP.

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Objective: To explore the effects of Hongjing-1 Recipe (HJ-1) on erectile function and the expression of the gap junction protein Connexin43 (Cx43) in the penile tissue in male rats with bilateral cavernous nerve injury (BCNI).

Methods: Fifty male SD rats were randomly divided into five groups of an equal number: sham operation, BCNI model control, and low-, medium- and high-dose HJ-1. The BCNI model was made in the latter four groups by clamping the bilateral cavernous nerves with hemostatic forceps.

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Neurogenic erectile dysfunction (NED) is an inevitable postoperative disease of cavernous nerve injury which will lead to various pathophysiological changes in the corpus cavernosum and dorsal penile nerve caused by radical prostatectomy (RP). Although serval years of clinical application of HJIG I granules (HJIG), an innovative formulation, has demonstrated its reliable clinical efficacy against NED, the mechanism of HJIG remains unclear. This study aimed to assess the neuroprotective effect of HJIG, to repair damaged nerves in a rat model of bilateral cavernous nerve injury (BCNI) in vivo and their effects on neurites of major pelvic ganglia (MPG) regeneration and Schwann cells (SCs) proliferation in vitro.

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Sonic hedgehog (Shh) is an important regulator of penile erectile function in adult males, and abnormal Shh signals may be involved in the mechanisms of ED. Current studies on the relationship of the Shh signaling pathway with ED are mainly concentrated on neurogenic ED caused by bilateral cavernous nerve injury, diabetes-induced endocrinological ED, and senile ED. This review focuses on the changes of the Shh signaling pathway in different types of ED and clarifies the mechanisms of the Shh signaling pathway regulating ED, hoping to give some inspiration to further related studies.

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Objective: To explore the regulatory effect of salidroside on H2O2-induced decrease in the expression of the connexin43 (Cx43) protein in corpus cavernosum smooth muscle cells (CCSMC).

Methods: Rat CCSMCs were isolated, primarily cultured in vitro and identified by immunocytochemical assay. The optimum concentration of H2O2 for intervention was determined by detecting its effect on the viability of the CCSMCs and used in the treatment of the CCSMCs for different lengths of time, and meanwhile salidroside was applied at 16 μg/ml (low dose) or 64 μg/ml (high dose) for intervention.

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Article Synopsis
  • HongJing I (HJI) is a traditional Chinese herbal remedy that has shown promise in treating erectile dysfunction (ED) but its exact mechanism of action is not fully understood.
  • In a study with rats that underwent bilateral cavernous nerve injury, HJI was administered in varying doses over 28 days, showing significant improvement in intracavernous pressure (ICP) compared to the control group.
  • The research indicated that HJI may help relieve ED by reducing cavernosum fibrosis and inhibiting RhoA/ROCK2 signaling pathways, although more studies are needed to clarify these mechanisms.
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Erectile dysfunction (ED) is closely related with the phenotypic modulation of corporal cavernosum smooth muscle cells (CCSMC), a transitional tendency of CCSMCs switching from the contractile phenotype to the synthetic or proliferative phenotype. The molecular markers of contractile CCSMCs include α-SMA, SMMHC, Calponin, Smoothelin, and Desmin, while those of synthetic or proliferative CCSMCs involve Vimentin, Osteopontin, and Collagen I. Current studies show that phenotypic transformation of CCSMCs is related to the pathophysiological processes of different types of ED, such as bilateral cavernous nerve injury-induced ED, diabetes mellitus-associated ED, arterial ED, hypertension-associated ED, and so on.

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