Quercetin boosts nitric oxide levels and modulates the activities of arginase, acetylcholinesterase and adenosine deaminase in the <i>corpus cavernosum</i> of cyclosporine‐treated rats
Ayodeji A. Olabiyi, Olamide S. Tope‐Eniola, Adedotun Olayemi Oluwatuyi, Oluwafunmilayo Alabi, Olaoluwa G. Ademola, Opeyemi M. Oguntimehin, Yemisi R. AlliSmith
Abstract
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.