ABSTRACT
OBJECTIVES: We aim to evaluate the effect of ischemic preconditioning (IPreC) on testicular tissue after transient middle cerebral artery occlusion (MCAo) in Streptozotocin-induced diabetic (STZ) and non-diabetic rats. METHODS: Testis injury and alterations of testosterone levels were evaluated histologically.. Testicular damage was detected by using hematoxylin- eosin and periodic acid- schiff staining and apoptosis was identified by terminal-deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL). RESULTS: Total mean serum testosterone levels decreased in all diabetic groups (p < 0.05) although remote ischemia and IPreC did not have any effect. Serious testicular tubular damage was observed in both, diabetic and ischemic groups (p 0.05). Otherwise, remote IPreC induced MNAC instead of any changes in histopathological architecture. Moreover, remote IPreC reduced the tubular degeneration against synergistic damage of both ischemia and diabetes (p < 0.05). CONCLUSIONS: It can be suggested that remote ischemic preconditioning prevents testicular damage by improving histopathological alterations and inducing apoptosis, probably temporarily, after focal transient middle cerebral artery occlusion in both, diabetic and non-diabetic rats. This is the first report demonstrating protective effects of ischemic preconditioning on remote testis injury after transient middle cerebral artery occlusion in diabetic rats (Fig. 6, Ref. 23).
Subject(s)
Diabetes Mellitus, Experimental/metabolism , Infarction, Middle Cerebral Artery/metabolism , Ischemic Preconditioning , Testicular Diseases/metabolism , Animals , Apoptosis , Case-Control Studies , Diabetes Mellitus, Experimental/complications , In Situ Nick-End Labeling , Infarction, Middle Cerebral Artery/complications , Infarction, Middle Cerebral Artery/pathology , Ischemia/etiology , Ischemia/metabolism , Ischemia/pathology , Male , Rats , Rats, Sprague-Dawley , Testicular Diseases/etiology , Testicular Diseases/pathology , Testosterone/metabolismABSTRACT
INTRODUCTION: Ischemic preconditioning (IPreC) can render the brain more tolerant to a subsequent potential lethal ischemic injury. Hyperglycemia has been shown to increase the size of ischemic stroke and worsen the clinical outcome following a stroke, thus exacerbating oxidative stress. Adropin has a significant association with cardiovascular disease, especially with diabetes. In this study, we aimed to evaluate the role of the IPreC due to modulating the expression of adropin and oxidative damage markers against stroke by induced transient middle cerebral artery occlusion (MCAo) in streptozotocin (STZ)-induced diabetic rats. MATERIAL-METHOD: 72 male Spraque Dawley rats were allocated to 8 groups. In order to evaluate alterations of anti/oxidative status and adropin level, we induced transient MCAo seven days after STZ-induced diabetes. Also we performed IPreC 72h before transient MCAo to assess whether IPreC could have a neuroprotective effect against ischemia-reperfusion injury. RESULTS: The general characteristics of STZ-treated rats (STZ) included reduced body weight and elevated blood glucose levels compared to non-diabetic ones. Ischemic preconditioning before cerebral ischemia significantly reduced infarction size compared with the other groups [IPreC+MCAo (27±11mm(3)) vs. MCAo (109±17mm(3)) p<0.001; STZ+IPreC+MCAo (38±10mm(3)) vs. STZ+MCAo (165±45mm(3)) p<0.001, respectively]. The mean total antioxidant status level in IPreC groups was higher than other groups (p≤0.05). Moreover, IPreC considerably decreased mean adropin levels compared with other groups (p≤0.05). CONCLUSION: The study results supported the neuroprotective effects of ischemic preconditioning in MCA infarcts correlated with the level of oxidative damage markers and adropin.
