AB67. Molecular mechanisms of Chinese herbal formula Shuganyiyang (SGYY) capsule of treating arteriogenic erectile dysfunction (ED) in a rat model

OBJECTIVE: In this research, we use the rat model of arteriogenic erectile dysfunction to study the molecular mechanism of the treatment of erectile dysfunction with Shuganyiyang capsule. From the aspects of regulating relaxation and contraction signaling transduction in the smooth muscle of corpus cavernosum, the expression of connexin and vascular blood vessel endothelium cytokines. METHODS: Bilateral ligation of the internal iliac artery was performed on three-month old male Sprague-Dawley rats as an experimental group. The control group was underwent dissection of the internal iliac artery without ligation. Rats in the experimental group were divided into model group, sidenafil group, SGYY low-dosage group (0.5g/kg/d) and high-dosage group (1g/kg/d). After 30 days therapeutic course, expression of mRNA and protein of NOS/cGMP passageway and RhoA/ROCK passageway moleculars, expression of CX43, ET and some vascular blood vessel endothelium cytokines such as VEGF, IGF, TGF-h as VEGFendotheliumNA and protein of NOS/cGMP passageway and RhoA/ROCK passageway moleculars, ex RESULTS: Expression of eNOS, cGMP were significantly enhanced both in sidenafil group and in SGYY treatment groups (P<0.05). While PDE5 expression was significantly decreased in sidenafil group and SGYY treatment groups (P<0.05). There was no difference between SGYY high-dosage group and sidenafil group (P>0.05); Expression of VEGF, IGF, TGF-β were significantly enhanced in SGYY treatment groups (both high-dosage and low-dosage) (P<0.05). Akt mRNA expression and p-Akt/Akt protein expression were significantly enhanced in the treatment groups too (P<0.05); Plasma concentration of ET-1 was decreased in SGYY treatment groups compared to the model group (in high-dosage group P<0.05, in low dosage group P<0.01). Expression of ET mRNA in penis tissue of rats was decreased in SGYY treatment groups compared to the model group (P<0.01). Expression of CX43 mRNA was increased in the SGYY treatment groups compared to the model group (P<0.01); RhoA, ROCK expression in the treatment groups were significantly enhanced compared to the model group (in high-dosage group P<0.01, in low dosage group P<0.05). CONCLUSIONS: SGYY can improve the expression of NOS/cGMP passageway moleculars such as eNOS, cGMP in rat model with arteriogenic erectile dysfunction. Meanwhile, it can inhibit the expression of PDE5. It can improve the expression of vascular blood vessel endothelium cytokines and the related signaling transduction molecular Akt. It also can improve the expression of CX43, and decrease the expression of ET in rat model with arteriogenic erectile dysfunction, regulating the function of RhoA/ROCK passageway, which is the main signaling transduction of corpus cavernosum smooth muscle contraction. All of the above show the main mechanisms of SGYY capsule of treating AED in rat model.