Phenotypic modulation of Corpus Cavernosum Smooth Muscle Cells (CCSMCs) is an important step in the development and progression of bilateral cavernous nerve injury induced erectile dysfunction (BCNI-ED). To investigate the effect of exogenous hydrogen sulfide (H₂S) on the phenotypic modulation of CCSMCs in BCNI-ED rats, a total of 18 male Sprague-Dawley rats were equally divided into 3 groups, including sham-operated (Sham) group, BCNI group and BCNI treated with NaHS (BCNI + NaHS) group. The treated group received intraperitoneal injection of NaHS (100 μmol kg⁻¹day⁻¹) for 4 weeks starting day 1 postoperatively. Erectile function was measured by the ratio of intracavernous pressure (ICP)/mean arterial pressure (MAP), and relevant tissues were harvested for Immunohistochemistry, Hematoxylin and eosin (H&E), Masson's trichrome staining, H₂S fluorescent probe WSP-1 and Western blot. The primary CCSMCs were isolated and pretreatment with NaHS before exposed to PDGF-BB (platelet-derived growth factor). Relative expression mRNA and protein of phenotypic biomarkers, RhoA, ROCK-1 and cell cycle proteins were detected. Cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE), 3-mercaptopyruvate sulfurtransferase (3-MST) and H₂S levels in penile tissue was significantly decreased in the BCNI group compared with the Sham group. Compared with the BCNI group, administration of NaHS significantly increased the ratio of ICP/MAP, ratio of smooth muscle to collagen, expressions of a-SMA, calponin and decreased the expression of OPN, collagen-I, RhoA, ROCK1 in the penile tissue. PDGF-BB-treated CCSMCs exhibited higher expression of OPN, RhoA, ROCK1, and lower α-SMA, calponin, which were attenuated by NaHS pretreatment. NaHS suppressed RhoA/ROCK activity and decreased the expression of CDK2, Cyclin E₁, while increased the expression of P27^kip1 induced by PDGF-BB in CCSMCs. Taken together, this study indicated that exogenous H₂S inhibited the phenotypic modulation of CCSMCs by suppressing RhoA/ROCK1 signaling and affecting its downstream factor, CDK2, Cyclin E_1, P27^kip1, thereby improved BCNI rat erectile function.

海绵体平滑肌细胞（CCSMCs）的表型调节是双侧海绵体神经损伤引起的勃起功能障碍（BCNI-ED）发生和发展的重要步骤。为了研究外源性硫化氢（H ₂ S）对BCNI-ED大鼠CCSMCs表型调节的影响，将18只雄性Sprague-Dawley大鼠平均分为3组，包括假手术（Sham）组， BCNI组和BCNI用NaHS（BCNI + NaHS）组治疗。治疗组接受腹腔注射NaHS（100μmolkg ^-1天^-1），从术后第1天开始持续4周。通过腔内压力（ICP）/平均动脉压（MAP）的比值测量勃起功能，并收集相关组织进行免疫组织化学，苏木精和曙红（H＆E），Masson三色染色，H ₂ S荧光探针WSP-1和Western污点。分离主要的CCSMC，并在暴露于PDGF-BB（血小板衍生的生长因子）之前用NaHS进行预处理。检测表型生物标志物，RhoA，ROCK-1和细胞周期蛋白的相对表达mRNA和蛋白。胱硫醚-β-合酶（CBS）和胱硫醚-γ-裂合酶（CSE），3-巯基丙酮酸硫转移酶（3-MST）和H ₂与假手术组相比，BCNI组的阴茎组织中的S水平显着降低。与BCNI组相比，NaHS的给药显着增加了阴茎组织中ICP / MAP的比率，平滑肌与胶原的比率，α-SMA，钙蛋白的表达，并降低了OPN，胶原I，RhoA，ROCK1的表达。 。PDGF-BB处理的CCSMC表现出较高的OPN，RhoA，ROCK1表达和较低的α-SMA钙蛋白，这些均被NaHS预处理所减弱。NaHS抑制CCSMCs中RhoA / ROCK活性并降低CDK2，Cyclin E ₁的表达，同时增加PDGF-BB诱导的P27 ^kip1的表达。两者合计，这项研究表明外源H ₂S通过抑制RhoA / ROCK1信号传导并影响其下游因子CDK2，Cyclin E _1， P27 ^kip1而抑制CCSMC的表型调节，从而改善了BCNI大鼠的勃起功能。