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.
Andrology. 2022 Sep;10(6):1208-1216. doi: 10.1111/andr.13218. Epub 2022 Jul 11.
Erectile function is usually impaired after radiation therapy in prostate cancer patients. eNOS is a key enzyme in the process of erection. Mitochondria-associated membranes (MAMs) are closely contacted with the production and bioactivity of eNOS.
To study the mechanism of icariin improves the erectile function of rats treated with prostate radiation by controling the expression of MAMs in penile corpus cavernosum.
Twenty 8-week-old healthy male SD rats were randomized to four groups: control group, radiation therapy (RT) group, icariin (10 mg/kg/d gavage) group, and RT + icariin (10 mg/kg/d gavage) group (n = 5). In RT group and RT + icariin group, rats were irradiated with X-rays to the prostate region (total dose 37.5 gray; 7.5 gray/day for 5 days). The maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP), NO concentration and the level of IP R1, PACS2, FACL4, nNOS, p-eNOS, and eNOS in rats' penile cavernous tissue was determined 9 weeks after radiation therapy.
Compared with the control group and the RT + icariin group, the ICPmax/MAP of the RT group was remarkably reduced (p < 0.05). The levels of p-eNOS/eNOS, nNOS and the concentration of NO in the penile cavernous tissue of the penis in the RT group were remarkably decreased compared to the control group and the RT + icariin group (p < 0.05). The levels of IP R1, PACS2, and FACL4 in penile cavernous tissue of the RT group were significantly higher than those in the control group and the RT + icariin group (p < 0.05).
After prostate X-ray radiotherapy in rats, the formation of MAMs may be increased by increased expression of IP R1, PACS2, and FACL4 in penile cavernous tissue, resulting in impaired erectile function. Icariin might increase p-eNOS/eNOS and improve erectile function in rats after prostate radiotherapy by inhibiting the expression of IP R1, PACS2, and FACL4.
前列腺癌患者在接受放射治疗后，勃起功能通常会受损。eNOS 是勃起过程中的关键酶。线粒体相关膜（MAMs）与 eNOS 的产生和生物活性密切相关。
通过控制阴茎海绵体中 MAMs 的表达，研究淫羊藿苷改善前列腺放射治疗大鼠勃起功能的机制。
将 20 只 8 周龄健康雄性 SD 大鼠随机分为 4 组：对照组、放射治疗（RT）组、淫羊藿苷（10mg/kg/d 灌胃）组、RT+淫羊藿苷（10mg/kg/d 灌胃）组（n=5）。在 RT 组和 RT+淫羊藿苷组中，对大鼠前列腺区域进行 X 射线照射（总剂量 37.5 戈瑞；5 天，每天 7.5 戈瑞）。放射治疗 9 周后测定大鼠阴茎海绵体最大腔内压/平均动脉压（ICPmax/MAP）、NO 浓度及 IP R1、PACS2、FACL4、nNOS、p-eNOS、eNOS 水平。
与对照组和 RT+淫羊藿苷组相比，RT 组的 ICPmax/MAP 显著降低（p<0.05）。与对照组和 RT+淫羊藿苷组相比，RT 组阴茎海绵体组织中 p-eNOS/eNOS、nNOS 和 NO 浓度显著降低（p<0.05）。RT 组阴茎海绵体组织中 IP R1、PACS2 和 FACL4 的水平明显高于对照组和 RT+淫羊藿苷组（p<0.05）。
在大鼠前列腺 X 射线放疗后，阴茎海绵体组织中 IP R1、PACS2 和 FACL4 的表达增加，可能导致 MAMs 的形成增加，从而导致勃起功能障碍。淫羊藿苷可能通过抑制 IP R1、PACS2 和 FACL4 的表达，增加 p-eNOS/eNOS，改善前列腺放射治疗后大鼠的勃起功能。
