Quercetin boosts nitric oxide levels and modulates the activities of arginase, acetylcholinesterase and adenosine deaminase in the corpus cavernosum of cyclosporine-treated rats.

One of the primary causes of erectile dysfunction (ED) in males is cardiovascular disease, such as hypertension (HT). As a result, the goal of this study is to see how quercetin (Q) affects the important biochemical parameters (nitric oxide, endogenous antioxidant enzymes)/specific enzymes (arginase, acetylcholinesterase and adenosine deaminase) linked to be responsible for smooth muscle relaxation in respect to sexual function. Wistar male rats (30) weighing 200-250 g were placed into five groups at random as follows: normal control group given normal saline (CTRL), hypertensive rats administered 25 mg/kg/day cyclosporine classified as ED group (HT), positive control administered Sildenafil (SIL, 5 mg/kg/day), quercetin (Q) 25 mg/kg/day (25 Q) and Q 50 mg/kg/day (50 Q). For 30 days, cyclosporine was administered i.p., while Q therapy was orally. HT was confirmed before the Q therapy after which the experimental rats were subjected to euthanasia. Nitric oxide (NO) levels, as well as enzymes [Superoxide dismutase, catalase, arginase, acetylcholinesterase (AChE) and adenosine deaminase (ADA)], were measured in the corpus cavernosum. Cyclosporine elevated arginase, AChE and ADA activity while lowering NO levels. Compared to the control group, Q of both concentrations reduced the activity of these enzymes and improved antioxidant status and NO levels. Thus, one of the mechanisms of action via which Q acts in the management of ED could be its ability to modulate these important enzymes and boost NO production.