Yueyang Zhang1, Changting Huang2, Shaoming Liu3, Jianqi Bai4, Xiaojing Fan5, Jun Guo6, Yingyu Jia7, Zhijie Zhang8, Xiaojun Chen8, Yusen Jia8, Ping Zhang4, Bin Wang9, Xiuju Zhang10. 1. Department of Andrology, Wangjing Hospital of China Academy of Traditional Chinese Medicine Beijing 100102. 2. Department of Pediatrics, Wangjing Hospital of China Academy of Traditional Chinese Medicine Beijing 100102. 3. Department of Urology, Third Affiliated Hospital of Beijing University of Chinese Medicine Beijing 100029. 4. Department of Pathology, Wangjing Hospital of China Academy of Traditional Chinese Medicine Beijing 100102. 5. Department of Acupuncture and Moxibustion, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine Tianjin 300150. 6. Department of Andrology, Xiyuan Hospital of China Academy of Traditional Chinese Medicine Beijing 100091. 7. Department of Scientific Research, Wangjing Hospital of China Academy of Traditional Chinese Medicine Beijing 100102. 8. Department of Urology, Oriental Hospital of Beijing University of Chinese Medicine Beijing 100078. 9. Department of Andrology, Dongzhimen Hospital of Beijing University of Chinese Medicine Beijing 100700. 10. Department of Traditional Chinese Medicine, Pinggu District Hospital Beijing 101200.
Abstract
OBJECT: Oxidative stress involved in the regulation of arterial erectile dysfunction (A-ED). Previously report have indicated that quercetin have an antioxidant effect. In the current study, we have established the rats' model for study the therapeutic effect of quercetin on A-ED and further investigated the molecular mechanism of action. METHODS: Wistar rats were divided into sham group, A-ED group, A-ED group with low dose of quercetin, and A-ED group with high dose of quercetin. Intracavernous pressure (ICP) and mean arterial pressure (MBp) are two important indicators used for evaluation the A-ED. The changes of ICP and MBp were determined by cavernous nerve electrostimulation after treatment of quercetin at indicated doses. The expression of nitric oxide synthase (NOS) subtypes was detected by RT-PCR and Western blotting. RESULTS: Our results indicated that ICP was significantly reduced in A-ED rats model compared with sham group, and was significantly increased after quercetin treatment (P < 0.01), while no significant effect on the MBp. The data also showed that sGC inhibitor ODQ and NOS inhibitor LNNA can significantly inhibited the ICP which induced by quercetin. These results suggest that NO-cGMP signaling pathway plays a crucial role in A-ED. Then, we found that the mRNA and protein levels of eNOS were significantly reduced in A-ED group compared with sham group. After treated with quercetin may cause the eNOS RNA and protein were significantly up-regulated (P < 0.01), showing a dose-dependent effect. iNOS expression have a certain degree of increased after quercetin treatment. nNOS expression was not significantly increased before and after treated with quercetin. In a word, quercetin can improved the A-ED by up-regulated ICP, which related to up-regulation of NO-cGMP signaling pathway. CONCLUSION: Preliminary results of this study suggested that quercetin protected expression and function of eNOS in cavernous endothelial cells, and restored part of normal function of NO-cGMP pathway in the process of penis erection.
OBJECT: Oxidative stress involved in the regulation of arterial erectile dysfunction (A-ED). Previously report have indicated that quercetin have an antioxidant effect. In the current study, we have established the rats' model for study the therapeutic effect of quercetin on A-ED and further investigated the molecular mechanism of action. METHODS:Wistar rats were divided into sham group, A-ED group, A-ED group with low dose of quercetin, and A-ED group with high dose of quercetin. Intracavernous pressure (ICP) and mean arterial pressure (MBp) are two important indicators used for evaluation the A-ED. The changes of ICP and MBp were determined by cavernous nerve electrostimulation after treatment of quercetin at indicated doses. The expression of nitric oxide synthase (NOS) subtypes was detected by RT-PCR and Western blotting. RESULTS: Our results indicated that ICP was significantly reduced in A-ED rats model compared with sham group, and was significantly increased after quercetin treatment (P < 0.01), while no significant effect on the MBp. The data also showed that sGC inhibitor ODQ and NOS inhibitor LNNA can significantly inhibited the ICP which induced by quercetin. These results suggest that NO-cGMP signaling pathway plays a crucial role in A-ED. Then, we found that the mRNA and protein levels of eNOS were significantly reduced in A-ED group compared with sham group. After treated with quercetin may cause the eNOS RNA and protein were significantly up-regulated (P < 0.01), showing a dose-dependent effect. iNOS expression have a certain degree of increased after quercetin treatment. nNOS expression was not significantly increased before and after treated with quercetin. In a word, quercetin can improved the A-ED by up-regulated ICP, which related to up-regulation of NO-cGMP signaling pathway. CONCLUSION: Preliminary results of this study suggested that quercetin protected expression and function of eNOS in cavernous endothelial cells, and restored part of normal function of NO-cGMP pathway in the process of penis erection.