Veterinary Research Forum

Abstract Buildup of reactive oxygen species during testicular torsion causes oxidative stress and ischemia-reperfusion (I/R) injury in testis. The purpose of this study was to investigate influence of β-cryptoxanthin (BCX) on I/R injury in testicular torsion/detorsion in mature rats. Thirty mature male Wistar rats were divided into five groups of six animals each, including sham group: In this group, midline incision of the scrotum was performed and the testicles were taken out for 2 hr with a 720-degree rotation, I/R group: In this group, midline incision of the scrotum was performed and the testicles were taken out and undergone ischemia for 2 hr with a 720-degree rotation, I/R/Oil group: In this group, a midline scrotum cut was performed, the testicles were taken out, ischemia was created for 2 hr with a 720-degree rotation, and at the end of ischemia 100 µL of corn oil (BCX solvent) was injected intraperitoneally, I/R/BCX10 group: The same as I/R/Oil group, as well as intraperitoneal administration of 100 µL of BCX (10.00 µg kg^-1) at the end of ischemia, and I/R/BCX40: The same as I/R/Oil group, as well as intraperitoneal administration of 100 µL of BCX (40.00 µg kg^-1) at the end of ischemia. Evaluations were based on histopathological and spermatological parameters and oxidative stress assessments. Histopathological spermatological and oxidative stress parameters values obtained from I/R/BCX40 were significantly different from those of other groups (p < 0.05). It could be concluded that BCX could ameliorate testicular injuries in acute testicular torsion/detorsion in mature rats.

Abstract This study was performed to evaluate the role of electroacupuncture on kidney 1 (Ki1) acupoint to prevent the heart and brain injury following ischemia/reperfusion of both kidneys. 24 Sprague Dawley rats were randomly assigned into four equal groups. In the treatment 1 group, following anesthesia, acupuncture needles were inserted on Ki1 on the palm of both hindlimbs and connected to electroacupuncture unit for a 3.00 Hz direct current, 1 hr before surgery until the end of surgery. In treatment two groups, the electroacupuncture was also performed 48 and 24 hr before the operation, with the same protocol as treatment 1. Control 1 and control 2 groups had the same procedures like the treatment ones, except for acupuncture. Immediately after reperfusion, the samples of brains and hearts were taken and prepared for microscopic examination. Histopathological study of the heart in the control and treatment groups showed the breakage of myofibrils, hyaline necrosis, edema and disorganization of myocytes. The severity of cardiac lesions was decreased in both treatment groups in comparison with the controls. Brain in control and treatment groups showed ischemic necrosis, disorganization of the neurons in the hippocampus, and edema. The severity of lesions was reduced in the treatment groups and showed a significant difference between the control and treatment 1. It could be concluded that electroacupuncture on the Ki1 point could reduce the severity of damages induced by renal ischemia/reperfusion in the remote organs of the heart and brain.

Abstract The present study aimed to evaluate the protective effect of gallic acid on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rat. Forty male rats were randomly divided into sham, control (I/R injury) and three gallic acid-pretreated groups. To induce I/R lesions, the celiac artery was clamped for 30 min and then the clamp was removed to allow reperfusion for 6 hr. Pretreated rats received gallic acid (15, 30 or 60 mg kg^-1, intraperitoneally) 30 min prior to the induction of I/R injury. Macroscopic and microscopic evaluations of the areas of ulceration were compared. Samples of gastric mucosa were collected to evaluate the protein expression of pro-apoptotic factor, caspase-3, and pro-inflammatory enzyme, inducible nitric oxide synthase (iNOS) using western blot. Pretreatment with gallic acid decreased the total area of gastric lesions. Gallic acid at 30 mg kg^-1 decreased the levels of protein expression of caspase-3 and iNOS induced by I/R injury. Our findings showed the protective effect of gallic acid on gastric mucosa against ischemia-reperfusion injury. This effect of gallic acid was mainly mediated by reducing protein expression of iNOS and caspase-3.