Yuan Piao, Li Xiong, Xiong Wen-Ju, Jiang Jun, Jiang Rui
Department of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Department of Thyroid Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Sex Med. 2023 Jun 20;11(3):qfad029. doi: 10.1093/sexmed/qfad029. eCollection 2023 Jun.
The relationship between galanin and erectile function under low androgen levels is still unclear.
To explore whether a low testosterone level damages the erection of a rat by regulating the expression of galanin and GalR in penile cavernous tissue.
Thirty-six male Sprague-Dawley rats, 8 weeks of age, were randomly grouped as follows (n = 6): control, castration, castration + testosterone replacement, control + transfection, castration + transfection, and castration + empty transfection. At 4 weeks after castration, rats in the transfection group were injected with lentivirus carrying the targeting galanin gene (2 × 10 TU/mL, 10 μL) in the corpus cavernosum. After 1 week of injection, the intracavernosal pressure (ICP), mean arterial blood pressure (MAP), nitric oxide (NO), serum testosterone concentration, galanin, GalR1-3, ROCK1, ROCK2, and p-eNOS/eNOS in the rat penile tissues were evaluated.
ICPmax/MAP and the expression of galanin in the corpus cavernosum in castrated rats were obviously decreased as compared with those in the control rats.
The castrated rats showed remarkably lower ICPmax/MAP, galanin, GalR1-3, p-eNOS/eNOS, and NO content and markedly higher ROCK1 and ROCK2 in penile tissues than the control group ( < .05). The transfected rats administrated with LV Gal had obviously higher ICPmax/MAP, p-eNOS/eNOS, and NO content and less ROCK1 and ROCK2 protein expression in the corpus cavernosum when compared with the castration group ( < .05).
Upregulating the expression of galanin in the penile corpus cavernosum might be a novel method of treating erectile dysfunction caused by a low androgen level.
The conclusions obtained in the animal experiments need to be confirmed in human data.
The erectile function of hypoandrogen rats might be inhibited by downregulating the level of galanin and GalR1-3, upregulating ROCK1 and ROCK2 levels, and inhibiting the eNOS/NO signaling pathway in penile corpus cavernosum.
低雄激素水平下甘丙肽与勃起功能之间的关系仍不清楚。
探讨低睾酮水平是否通过调节阴茎海绵体组织中甘丙肽和甘丙肽受体（GalR）的表达来损害大鼠勃起功能。
将36只8周龄雄性Sprague-Dawley大鼠随机分为以下几组（n = 6）：对照组、去势组、去势+睾酮替代组、对照组+转染组、去势+转染组、去势+空载体转染组。去势4周后，给转染组大鼠阴茎海绵体内注射携带靶向甘丙肽基因的慢病毒（2×10 TU/mL，10 μL）。注射1周后，评估大鼠阴茎组织中的海绵体内压（ICP）、平均动脉血压（MAP）、一氧化氮（NO）、血清睾酮浓度、甘丙肽、GalR1-3、Rho相关卷曲螺旋蛋白激酶1（ROCK1）、Rho相关卷曲螺旋蛋白激酶2（ROCK2）以及磷酸化内皮型一氧化氮合酶/内皮型一氧化氮合酶（p-eNOS/eNOS）。
与对照组相比，去势大鼠的ICPmax/MAP以及阴茎海绵体中甘丙肽的表达明显降低。
去势大鼠阴茎组织中的ICPmax/MAP、甘丙肽、GalR1-3、p-eNOS/eNOS和NO含量显著低于对照组，而ROCK1和ROCK2明显高于对照组（P < 0.05）。与去势组相比，注射携带甘丙肽基因慢病毒的转染大鼠阴茎海绵体中的ICPmax/MAP、p-eNOS/eNOS和NO含量明显更高，ROCK1和ROCK2蛋白表达更低（P < 0.05）。
上调阴茎海绵体中甘丙肽的表达可能是治疗低雄激素水平所致勃起功能障碍的新方法。
动物实验得出的结论需要在人体数据中得到证实。
低雄激素大鼠的勃起功能可能通过下调甘丙肽和GalR1-3水平、上调ROCK1和ROCK2水平以及抑制阴茎海绵体中的eNOS/NO信号通路而受到抑制。
