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低雄激素水平对大鼠阴茎海绵体组织瞬时受体电位通道表达的影响及其与勃起功能的关系。

Effect of low androgen levels on transient receptor potential channels expression in rat penile corpus cavernosum tissue and its relationship with erectile function.

机构信息

Department of Urology, the Affiliated Hospital of Southwest Medical University, Luzhou, China.

Department of Thyroid Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, China.

出版信息

Andrologia. 2022 Sep;54(8):e14477. doi: 10.1111/and.14477. Epub 2022 May 20.

DOI:10.1111/and.14477
PMID:35596534
Abstract

The exact mechanism by which testosterone deficiency causes ED has not yet been elucidated. TRPC is involved in the process of smooth muscle cell contraction and relaxation. The effect of androgens on TRPCs and their relationship with erectile function are currently unclear. Thirty male SD rats were randomly divided into six groups: control group, castration group, castration + testosterone (T) group (cast + T), control + transfection group (control + trans), control + empty transfection group and castration + transfection group (cast + trans). The transfection group rats were given with lentivirus (1 × 10 TU/mL, 15 μl) carrying the siRNA targeting TRPC4 gene in the rat penile cavernous tissue at 4 weeks after castration. The tests were performed at 5 weeks after castration. Comparing the cast group with the control, the ICPmax/MAP, p-eNOS/eNOS and NO levels in the rat penile tissue were significantly lower (p < 0.01) and the level of TRPC3, TRPC4 and TRPC6 in the rat penile tissue was significantly increased (p < 0.01). When the cast + trans group was compared to the cast group, ICPmax/MAP was markedly higher (p < 0.05), and the level of the TRPC4 was remarkably lower (p < 0.05). Low androgen levels might inhibit an erectile function through up-regulation of the expression of TRPC3, TRPC4 and TRPC6 in rat penile cavernous tissue. Inhibition the level of TRPC4 in rat penile tissue may improve the erectile function in low androgen levels.

摘要

确切的机制,其中睾丸激素缺乏导致 ED 尚未阐明。TRPC 参与平滑肌细胞收缩和舒张的过程。雄激素对 TRPCs 的影响及其与勃起功能的关系目前尚不清楚。30 只雄性 SD 大鼠随机分为 6 组:对照组、去势组、去势+睾酮(T)组(去势+ T)、对照组+转染组(对照组+转)、对照组+空转染组和去势+转染组(去势+转)。转染组大鼠在去势后 4 周时给予携带靶向大鼠阴茎海绵体组织中 TRPC4 基因的 siRNA 的慢病毒(1×10TU/mL,15μl)。去势后 5 周进行测试。与对照组相比,去势组大鼠阴茎组织中的 ICPmax/MAP、p-eNOS/eNOS 和 NO 水平明显降低(p<0.01),而阴茎组织中 TRPC3、TRPC4 和 TRPC6 的水平明显升高(p<0.01)。与去势组相比,去势+转染组大鼠的 ICPmax/MAP 明显升高(p<0.05),而 TRPC4 水平明显降低(p<0.05)。低雄激素水平可能通过上调大鼠阴茎海绵体组织中 TRPC3、TRPC4 和 TRPC6 的表达来抑制勃起功能。抑制大鼠阴茎组织中 TRPC4 的水平可能改善低雄激素水平下的勃起功能。

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