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目的:研究H2S信号通路在雄激素缺乏引起勃起功能下降中的作用。方法:8周龄健康雄性SD大鼠30只,随机分成6组:假手术2周组(A组)、假手术4周组(B组)、去势2周组(C组)、去势4周组(D组)、去势后雄激素替代治疗2周组(E组)和去势后雄激素替代治疗4周组(F组)。E、F去势术后给予生理剂量丙酸睾酮3 mg/(kg·d)皮下注射。测定各组大鼠血清睾酮、阴茎海绵体内压(ICP)、平均颈动脉压(MAP),测定血浆和阴茎组织内H2S浓度,免疫组化和Western印迹检测胱硫醚-β-合成酶(CBS)、胱硫醚-γ-裂解酶(CSE)蛋白的表达。结果:血清睾酮水平结果显示C组[(0.63±0.15)nmol/L]较A组[(16.55±4.17)nmol/L]、E组[(18.99±4.62)nmol/L]显著降低(P<0.05);D组[(0.70±0.22)nmol/L]较B组[(15.44±5.18)nmol/L]、F组[(20.99±6.41)nmol/L]显著降低(P<0.05)。予以5、7 V电刺激盆神经后,ICP/MAP在C组较A、E组显著降低(P<0.05),D组较B、F组显著降低(P<0.05)。血浆及阴茎组织内H2S浓度含量C组较A、E组显著降低(P<0.05),D组较B、F组显著降低(P<0.05)。免疫组化和Western印迹检测阴茎海绵体组织内CBS、CSE蛋白表达量,C组较A、E组显著降低(P<0.05),D组较B、F组显著降低(P<0.05)。C组较D组CBS、CSE蛋白表达量显著降低(P<0.05)。结论:阴茎海绵体组织CBS、CSE表达下降引起H2S信号通路受抑可能是雄激素缺乏引起大鼠勃起功能下降的机制之一。
AIM: To investigate the role of H2S signaling pathway in the decline of erectile function induced by androgen deficiency. Methods: Thirty male Sprague-Dawley rats, 8 weeks old, were randomly divided into 6 groups: sham operation for 2 weeks (group A), sham operation for 4 weeks (group B), castration for 2 weeks (group C) 4 weeks group (D group), 2 weeks after castration androgen replacement therapy group (E group) and 4 days after castration androgen replacement therapy group (F group). E, F After ovariectomy, physiological doses of testosterone propionate 3 mg / (kg · d) were injected subcutaneously. The levels of serum testosterone, penis and intracapsular pressure (ICP) and mean carotid artery pressure (MAP) were measured. The concentrations of H2S in plasma and penile tissue were measured. The expressions of cystathionine-β-synthase ), Cystathionine-γ-lyase (CSE) protein expression. Results: The level of serum testosterone in group C [(0.63 ± 0.15) nmol / L] was significantly lower than that in group A [(16.55 ± 4.17) nmol / L] and group E [(18.99 ± 4.62) nmol / L] 0.05). Compared with B group [(0.70 ± 0.22) nmol / L] in group D [(15.44 ± 5.18) nmol / L] and group F [(20.99 ± 6.41) nmol / L] After 5,7 V electrical stimulation of the pelvic nerve, the ICP / MAP in C group was significantly lower than that in A and E groups (P <0.05), and was significantly lower in group D than those in B and F groups (P <0.05). The contents of H2S in plasma and penile tissue in group C were significantly lower than those in groups A and E (P <0.05), but were significantly lower in group D than those in groups B and F (P <0.05). The expression of CBS and CSE in penis tissue were detected by immunohistochemistry and Western blotting. The expression of CBS and CSE in group C was significantly lower than that in group A and E (P <0.05), but significantly lower in group D than those in group B and F (P <0.05). The protein expression of CBS and CSE in group C was significantly lower than that in group D (P <0.05). CONCLUSIONS: The suppression of H2S signaling pathway caused by the decrease of CBS and CSE expression in the corpus cavernosum may be one of the mechanisms by which androgen deficiency can cause erectile dysfunction in rats.