Abstract
Tetracarpidium conophorum (walnut) is used in folk medicine for the treatment of erectile dysfunction but the mechanism remains unclear. This study evaluated the effect of aqueous extract from T conophorum leaves on oxidative stress-induced penile damage and key enzymes linked to erectile dysfunction. The inhibitory effect of the extract on sodium nitroprusside (SNP)-induced lipid peroxidation, arginase, angiotensin I-converting enzyme (ACE) and acetylcholinesterase (AChE) activities in penile and testicular tissue homogenates were determined via colorimetric method. The aqueous extract inhibited SNP-induced lipid peroxidation in rats penile and testicular homogenates in a dose dependent manner. The highest inhibitory effect was obtained in the penis at a concentration of 0.5 mg/mL. Furthermore, the extract inhibited arginase activity in a dose dependent pattern. The IC50 revealed that the extract had significantly (P
Highlights
Penile erection is a neurovascular event which depends on neural integrity, functional vascular system, and healthy cavernosal tissue (Bivalacqua et al, 2003)
This study evaluated the effect of aqueous extract from T. conophorum leaves on oxidative stress-induced penile damage and key enzymes linked to erectile dysfunction
Up-regulation of some enzymes such as arginase, acetylcholinesterase and angiotensin-I converting enzyme which are responsible for normal physiological processes in the penile and testicular vasculature could lead to erectile dysfunction (ED) via different mechanisms such as endothelial dysfunction, impairment of NO/cGMP pathway, smooth muscle dysfunction and neurodegeneration (Andersson, 2011)
Summary
Penile erection is a neurovascular event which depends on neural integrity, functional vascular system, and healthy cavernosal tissue (Bivalacqua et al, 2003). Up-regulation of some enzymes such as arginase, acetylcholinesterase and angiotensin-I converting enzyme which are responsible for normal physiological processes in the penile and testicular vasculature could lead to ED via different mechanisms such as endothelial dysfunction, impairment of NO/cGMP pathway, smooth muscle dysfunction and neurodegeneration (Andersson, 2011).
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