Xujun Yu , Jingyi Zhang , Suyun Xu , Jing Zhou , Chenglin Zhuang , Junjun Li , Baojun Zhuang
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引用次数: 0
Abstract
Background and aim
Guilingji capsules (GLJC) have the effect of treating erectile dysfunction (ED). This study aims to explore the potential mechanisms of GLJC in treating ED.
Experimental procedure
We conducted network pharmacology analysis of ED-related targets with GLJC components reported in the TCMSP database and GLJC components reported in the literature, respectively. Molecular docking was employed to validate the binding affinity of these molecular targets. Animal experiments were conducted to validate the aforementioned results. The mechanism of GLJC in treating ED was studied using d-galactose-induced aging rats, and orchiectomized rats were used to investigate further whether the mechanism of GLJC in treating ED is related to androgen.
Results and conclusions
Two network pharmacology analyses indicated that Androgen receptor (AR) and fibroblast growth factor 2 (FGF2) are the candidate targets, suggesting that the mechanism of ED treatment by GLJC may be related to androgens and angiogenesis. Molecular docking further validated the effective binding of GLJC components to these two targets. In animal experiments, GLJC significantly increased the frequency of erections and elevated serum free testosterone levels and penile tissue AR expression in aged rats. GLJC also promoted angiogenesis and inhibited penile tissue fibrosis in aged rats by regulating the expression of FGF2, RICTOR/P-AKT/P-FOXO1. However, such regulation was not observed in orchiectomized rats. Therefore, GLJC increased testosterone utilization in d-galactose-induced aging rats and regulated FGF2, RICTOR/P-AKT/P-FOXO1 signaling pathway in a T-dependent manner, promoting corpus cavernosum survival and angiogenesis. This mechanism led to the inhibition of penile fibrosis.
背景及目的：贵灵鸡胶囊具有治疗勃起功能障碍（ED）的作用。本研究旨在探讨GLJC治疗ed的潜在机制。实验步骤：我们分别用TCMSP数据库中报道的GLJC成分和文献中报道的GLJC成分对ed相关靶点进行网络药理学分析。通过分子对接验证这些分子靶点的结合亲和力。动物实验验证了上述结果。以d-半乳糖诱导的衰老大鼠为实验对象研究GLJC治疗ED的机制，并以去睾丸大鼠为实验对象进一步探讨GLJC治疗ED的机制是否与雄激素有关。结果和结论两项网络药理学分析显示雄激素受体（AR）和成纤维细胞生长因子2 （FGF2）是候选靶点，提示GLJC治疗ED的机制可能与雄激素和血管生成有关。分子对接进一步验证了GLJC组分与这两个靶点的有效结合。在动物实验中，GLJC显著增加了老龄大鼠的勃起频率，提高了血清游离睾酮水平和阴茎组织AR表达。GLJC还通过调节FGF2、RICTOR/P-AKT/ p - fox01的表达，促进老年大鼠血管生成，抑制阴茎组织纤维化。然而，在切除睾丸的大鼠中没有观察到这种调节。因此，GLJC增加了d-半乳糖诱导衰老大鼠的睾酮利用，并以t依赖的方式调节FGF2、RICTOR/P-AKT/P-FOXO1信号通路，促进海肌体存活和血管生成。这一机制导致了阴茎纤维化的抑制。
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