Mechanisms in Tridax procumbens leaf extract reversal of paroxetine-induced erectile dysfunction in corpus cavernosum of male Wistar rats

Abstract

Introduction: Aqueous leave extract of Tridax procumbens (AETPL) is reported to improve erectile functions; however, the mechanism is unclear. This study investigates the mechanism involved in the contractile activity of the corpus cavernosum after AETPL treatment of paroxetine-induced erectile dysfunctional adult male Wistar rats.

Methods: A total of 20 male Wistar rats were categorized into four groups of five and treated orally for four weeks: Group 1 (distilled water), Group 2 (paroxetine 10 mg/kg), Group 3 (paroxetine + AETPL 100 mg/kg), and Group 4 (paroxetine + Viagra 0.5 mg/kg). Contractile responses of excised corpus cavernosum strips (CS) were determined in response to acetylcholine (ACh), phenylephrine (PHE), potassium chloride (KCl), and calcium chloride (CaCl₂), and after incubation in L-NAME, indomethacin, nifedipine, adenosine, caffeine, nicorandil, and acetovanillone.

Results: The relaxation response (%) of CS to ACh was significantly inhibited in the paroxetine group compared to the AETPL- and the Viagra-co-treated group. Pre-incubation in L-NAME considerably enhanced the percentage relaxation in groups co-treated with AETPL and Viagra. Groups co-treated with AETPL and Viagra significantly inhibited contraction in response to cumulative doses of CaCl₂. Contractile responses of CS to cumulative doses of PHE after incubation in caffeine and adenosine were considerably inhibited in groups co-treated with AETPL and Viagra. Similarly, nicorandil (10^-4 M) enhanced the percentage relaxation to cumulative doses of ACh (10^-9 — 10^-5 M) in groups co-treated with AETPL and Viagra. The pre-incubation of CS with acetovanillone (10^-4 M) enhanced the percentage relaxation to ACh across groups.

Conclusion: Erectile dysfunction was reversed by AETPL-induced antioxidant/NADPH oxidase inhibitor activity, reduced calcium sensitivity, activation of ATP-sensitive K⁺ channel, and endothelial Nitric Oxide (NO) release.