| Part â… Effect of Apocynin on the erectile function of diabetic erectile dysfunction ratObjective:To investigate whether NADPH oxidase inhibitor Apocynin can ameliorate diabetes-related ED.Methods:In all,20male45-day-old Sprague-Dawley rats were divided into three groups. Group1included7age-matched control rats, Type1diabetes of other13rats were induced by a single intraperitoneal injection at dose of60mg/kg (Streptozotocin, STZ) in citrate buffer (50mM sodium citrate, pH4.5), as previously reported, blood glucose levels in serum samples obtained from the tail vein of all rats were detected before diabetes induction and after72h intraperitoneal injection of STZ with a blood glucose meter. The rats with blood glucose concentrations greater than16.7mmol/L were accepted as being diabetes. After8weeks,6diabetic rats were given saline by gavage for4weeks,7diabetic rats were given16mg/kg (10mM) per day of apocynin in saline by gavage for4weeks.7age-matched control rats were given saline for4weeks by gavage. At the end of treatment, a sample of blood was obtain from tail vein of all rats for measuring glucose levels which were considered as final blood glucose levels. Erectile responses were evaluated by determining mean arterial blood pressure (MAP) and intracavernosal pressure (ICP) with electrical stimulation of the cavernous nerve. The ratio of Maximum ICP-to-MAP (MaxICP/MAP) was the erectile function of rat.Results:The ratio of Maximum ICP-to-MAP (MaxICP/MAP) was significantly decreased in diabetic ED rats, compared to that of age-matched control rats (P<0.05). Apocynin improved erectile function of diabetic rats (P<0.05).Conclusions:Apocynin can ameliorate diabetes-related ED. Part â…¡NADPH oxidase inhibitor Apocynin decreasing the ROS production.Objective:To investigate whether NADPH oxidase inhibitor Apocynin can decrease the ROS production by inhibiting the expression of NADPH oxidase.Methods:NADPH oxidase subunit p47phox and p67phox were measured by Western Blot (WB). Reactive Oxygen Species (ROS) production was measured by dihydroethidium (DHE) staining and TBARS.Results:Expression levels of NADPH oxidase subunit p47phox and p67phox were increased in diabetic rats when compared to that of control rats (P<0.05), and it was noticed that Apocynin significantly reduced their expression levels in diabetic rats (P<0.05). ROS production was increased in diabetic rats when compared to that of control rats (P<0.05), the effect of Apocynin was a reduction in the ROS production in diabetic rats.Conclusions:NADPH oxidase inhibitor apocynin can decrease the ROS production by inhibiting the expression of NADPH oxidase. Part â…¢Effect of Apocynin on expression levels of nNOSand eNOSObjective:To investigate whether NADPH oxidase inhibitor Apocynin can improve the expression levels of nNOSand eNOS of diabetic rats.Methods:Expression levels of nNOSand eNOS were measured by Real-time PCR (RT-PCR), WB.Results:Expression levels of nNOS, eNOS were reduced in diabetic rats, compared to that of control rats (P<0.05). Apocynin significantly elevated their expression levels in diabetic rats (P<0.05).Conclusions:NADPH oxidase inhibitor apocynin can improve the expression levels of nNOSand eNOS of diabetic rats. Part â…£Effect of Apocynin on inhibiting the activity of RhoA/ROCK signaling pathwayObjective:To investigate whether NADPH oxidase inhibitor Apocynin can inhibit the activity of RhoA/ROCK signaling pathway.Methods:The levels of mRNA expression of RhoA,ROCK1and ROCK2were measured by RT-PCR. The levels of proteins expression of RhoA (cytosol), RhoA (membrane fraction), ROCK1, ROCK2and p-MYPT1were measured by WB.Results:The levels of mRNA expression of RhoA,ROCK1were increased in diabetic rats, compared to that of control rats (P<0.05). Apocynin significantly reduced their expression levels in diabetic rats (P<0.05). The levels of proteins expression of RhoA (membrane fraction), ROCK1and p-MYPT1were increased. Apocynin significantly reduced their expression levels in diabetic rats (P<0.05).Conclusions:NADPH oxidase inhibitor Apocynin can inhibiting the activity of RhoA/ROCK signaling pathway.
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