山海丹颗粒对勃起功能障碍模型大鼠的疗效及相关作用机制研究

The Curative Effect and Related Mechanism of Shanhaidan Granules on Rats with Erectile Dysfunction

  • 摘要:
      目的   观察山海丹颗粒对勃起功能障碍(Erectile dysfunction, ED)疾病的改善作用,并基于前期网络药理学分析结果,探讨可能的相关机制。
      方法   选取140只Wistar大鼠作为实验动物,雌雄各半。采用双侧髂内动脉结扎的方法,用雄性大鼠建立血管性ED动物模型,分为正常组、模型组、西地那非组、疏肝益阳胶囊组、山海丹颗粒低剂量组、山海丹颗粒中剂量组、山海丹颗粒高剂量组,给药组灌胃给药8周,正常组和模型组给予等体积的双蒸水。考察各组大鼠性行为学指标,TUNEL染色检测睾丸内生精细胞凋亡情况,Western blot和qPCR检测阴茎组织的iNOS、eNOS、nNOS和p38表达水平。
      结果   和模型组相比,山海丹颗粒显著缩短了ED大鼠的扑捉潜伏期和射精潜伏期,减少睾丸组织内凋亡的生精细胞数量,增加iNOS、eNOS、nNOS表达,抑制p38磷酸化。
      结论   山海丹颗粒可有效改善ED模型大鼠的疾病状态,其治疗ED的作用机制可能是通过调控iNOS、eNOS、nNOS和p38来实现的。

     

    Abstract:
      OBJECTIVE   To observe the effect of Shanhaidan Granules on erectile dysfunction (ED) disease, and to explore its possible related mechanisms based on the results of previous network pharmacological analysis.
      METHODS   140 Wistar rats were selected as experimental animals including 70 male rats and 70 female rats. Male rats were used to establish vascular ED animal models by bilateral internal iliac artery ligation, which were randomly divided into normal group, model group, sildenafil group, Shugan Yiyang capsule group, Shanhaidan granules low-dose group, medium-dose group and high-dose group. The normal group and the model group were given equal volumes of double distilled water. The sexual behavior indexes of rats in each group were investigated weekly. After 8 weeks of gavage, TUNEL staining was used to detect the apoptosis of spermatogenic cells in the testis. Western blot and qPCR were used to detect the expression levels of iNOS, eNOS, nNOS and p38 in penile tissues.
      RESULTS   Compared with the model group, Shanhaidan granules significantly shortened the capture latency and ejaculation latency of ED rats, reduced the number of apoptotic spermatogenic cells in the testicular tissue, increased the expressions of iNOS, eNOS, nNOS, and inhibited p38 phosphorylation.
      CONCLUSION   Shanhaidan granules can effectively improve the disease state of ED model rats, and its mechanism may be partly related to the regulation of iNOS, eNOS, nNOS and p38.

     

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