Abstract
Background: Ischemic preconditioning (IPC) is a brief episode of ischemia/reperfusion (I/R) that protects the brain from the damage induced by subsequent prolonged ischemia. Aim: To study the neuroprotective mechanism of IPC. Methods: 30 adult male Wistar rats (150-250 g) were divided into three groups 10 rats in each; the first group was sham-operated and served as a control, I/R group of rats subjected to 30 minutes of left common carotid artery occlusion (CCAO) followed by 24-hour of reperfusion, IPC group were treated with three episodes of 5-minutes of CCAO with 10 minutes of reperfusion in between, followed by 30 minutes of CCAO and then allowed for reperfusion for 24 hours. Neurobehavioral assessments were evaluated; Rhokinases (ROCK) and nitrite were measured in affected cerebral hemisphere. Results: Rats’ neurological deficits were significantly decreased in the I/R compared with the control group (P contrast, the ROCK level was significantly higher in I/R group compared to control group and its level significantly decreased in IPC rats when compared to I/R group (P 0.695, P = 0.000). Conclusions: Downregulation of ROCK level following preconditioning stimuli with the potential involvement of Nitric oxide (NO) appear to be one of the neuroprotective mechanisms of IPC protection against a subsequent I/R challenge evidence by improvement in the neurological deficits.
Highlights
Cerebral ischemic preconditioning (IPC) is an incident of brief episodes of ischemia that protects the brain from subsequent, more severe ischemic insult [1,2]
Ischemic preconditioning (IPC) rats showed a significant increase in nitrite (84.65 ± 12.61 μmol/l) when compared to both control and ischemia/reperfusion groups (56.03 ± 11.38, 59.18 ± 10.86 μmol/l respectively, P < 0.001), while no significant difference between the shamoperated and ischemia/reperfusion rats (Figure 3)
The current data demonstrated a significant increased in ROCK level in rats subjected to ischemia/reperfusion, these findings were further supported by Yano et al [26] and Li et al [27], Yano et al proved that Rho-kinase activity was increased in the ipsilateral cerebral hemisphere after 3 and 6 h but not 0.5 h compared with contralateral cerebral hemisphere in rats subjected to induced cerebral ischemia [26]
Summary
Cerebral ischemic preconditioning (IPC) is an incident of brief episodes of ischemia that protects the brain from subsequent, more severe ischemic insult [1,2]. Preconditioned brains actively suppressed genes that control metabolism, cell cycle regulation and ion channel activity indicating a complete reprogramming of the genomic response to ischemia. It results in shift the outcome from cell death to cell survival [8]. Ischemic preconditioning (IPC) is a brief episode of ischemia/reperfusion (I/R) that protects the brain from the damage induced by subsequent prolonged ischemia. Conclusions: Downregulation of ROCK level following preconditioning stimuli with the potential involvement of Nitric oxide (NO) appear to be one of the neuroprotective mechanisms of IPC protection against a subsequent I/R challenge evidence by improvement in the neurological deficits
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