The amelioration of testicular ischemia-reperfusion injury in rats by oxymatrine

Abstract

Introduction/Objective A crucial factor in testicular damage is the surplus of reactive oxygen species that arises from ischemia-reperfusion. Elevated levels of reactive oxygen species cause critical harm to cells. The present research focused on investigating the role of oxymatrine with antioxidative property in testicular ischemia-reperfusion injury induced by torsion and detorsion in a rat model.

Methods The study utilized a total of 60 rats, which were randomly assigned to one of three groups: a sham group with 20 rats, a testicular ischemia-reperfusion group with 20 rats, and a testicular ischemia-reperfusion group treated with oxymatrine, also consisting of 20 animals. Induction of testicular ischemia-reperfusion involved applying two hours of ischemia via 720° counterclockwise torsion to the left testis, with subsequent reperfusion initiated by detorsion. The activity of neutrophil nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a catalyst for reactive oxygen species production, the concentration of a prevalent reactive oxygen species indicator malondialdehyde, and spermatogenesis were all detected in left testicular tissues collected at the four hours or three months post-detorsion.

Results Testicular ischemia-reperfusion notably elevated NADPH oxidase activity and malondialdehyde content, while it adversely affected spermatogenesis in the testes (p < 0.001). Conversely, the administration of oxymatrine significantly lowered both NADPH oxidase activity and malondialdehyde concentration, and it also improved spermatogenic function in the testes (p < 0.001).

Conclusion We found that oxymatrine attenuates injury from testicular ischemia-reperfusion, and this effect operates by limiting reactive oxygen species production through NADPH oxidase activity inhibition.

Keywords: oxymatrine; testicular torsion; ischemia-reperfusion