Icariin inhibits the formation of mitochondria-associated membranes (MAMs) and improves erectile function in rats treated with prostate radiation.

Abstract

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 (10mg/kg/d gavage) group, and RT + icariin (10mg/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 IP3 R1, PACS2, FACL4, nNOS, p-eNOS, and eNOS in rats' penile cavernous tissue was determined 9weeks 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 IP3 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 IP3 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 IP3 R1, PACS2, and FACL4.