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Updated: Sep 6, 2025
Intracavernosal Pressure Recording to Evaluate Erectile Function in Rodents
Published on: June 6, 2018
Icariin inhibits the formation of mitochondria-associated membranes (MAMs) and improves erectile function in rats
Chang-Jian Deng1, Xiong Li1, Yang Zeng1
1Department of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Background:
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.
Objective:
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.
Methods:
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 IP3 R1, PACS2, FACL4, nNOS, p-eNOS, and eNOS in rats' penile cavernous tissue was determined 9 weeks after radiation therapy.
Results:
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).
Conclusions:
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.
Insights
Icariin improves erectile function in rats after prostate radiation therapy by regulating mitochondria-associated membranes (MAMs). This study shows icariin may reverse radiation-induced erectile dysfunction by inhibiting MAMs.
Area of Science:
- Urology
- Andrology
- Radiotherapy Research
Background:
- Radiation therapy for prostate cancer often impairs erectile function.
- Endothelial nitric oxide synthase (eNOS) is crucial for erections.
- Mitochondria-associated membranes (MAMs) influence eNOS production and activity.
Purpose of the Study:
- To investigate how icariin improves erectile function in rats post-prostate radiation.
- To determine if icariin modulates MAMs expression in penile tissue.
Main Methods:
- Rats received prostate radiation therapy (RT) with or without icariin.
- Erectile function was assessed by measuring maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP).
- Levels of key proteins (IP3R1, PACS2, FACL4, nNOS, p-eNOS, eNOS) and nitric oxide (NO) were quantified.
Main Results:
- RT significantly reduced ICPmax/MAP, nNOS, p-eNOS/eNOS, and NO concentration.
- RT increased IP3R1, PACS2, and FACL4 levels in penile tissue.
- Icariin treatment reversed these RT-induced changes.
Conclusions:
- Prostate radiation may increase MAMs formation via IP3R1, PACS2, and FACL4, leading to erectile dysfunction.
- Icariin may enhance erectile function post-radiotherapy by inhibiting IP3R1, PACS2, and FACL4, thereby improving eNOS activity.
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