Preconditioning by sub‐lethal ischemia/reperfusion or glibenclamide ameliorates lactate dehydrogenase activity to different extends in rat hippocampus and cerebral cortex (brain) subjected to ischemia/reperfusion injury

Abstract

Sub‐lethal short term ischemic exert adaptive responses which may protect from lethal ischemia, a phenomenon referred to as ischemia preconditioning (IPC). In the CNS, IPC causes increased tolerance to lethal ischemia reperfusion (I/R) injury; however, the precise mechanism is not fully understood. Similarly, glibenclamide, a selective blocker of K+(ATP) channels, was reported to protect against I/R injury via a preconditioning mechanism. Hence, the present study aimed to investigate the role of free radicals as well as pro‐ and anti‐inflammatory cytokines in rats exposed to a I/R injury. To this end, 32 male Wister Rats were divided into 4 groups, group I served as sham operated control, group II was subjected to 15 min ischemia by occlusion of both carotid arteries, followed by 60 min reperfusion, group III injected glibenclamide (1 mg/kg, i.p) 10 min before ischemia (15 min) followed by reperfusion (60 min), and in group IV, preconditioned (IPC) rats were subjected to 3 episodes of ischemia (3 min) followed by reperfusion (10 min) afterwards animals underwent ischemia (15 min) followed by reperfusion (60 min). I/R increased LDH activity, as well as lipid peroxides level, and decreased total antioxidant capacity (TAC) and IL‐10 level in the hippocampus; however, just cortical LDH and TCA levels were deranged. IPC and glibenclamide before I/R improved only LDH activity in the cerebral cortex and partly in the hippocampus. Hence, the study shows that both IPC and glibenclamide impart neuroprotection independent of free radical scavenging nor cytokine production in rats subjected to I/R injury.