Amelioration of Cerebral Ischemia reperfusion injury by Rosuvastatin via interference with inflammatory response and apoptosis
Objectives: The objective of this study is to investigate the possible cerebroprotective potential of rosuvastatin in brain ischemia reperfusion injury via interfering with inflammation and oxidative pathway and apoptosis. Materials and Methods: Adult albino rats were randomized into four groups as follow: Group (1) sham group: the rats were subjected to the same surgical procedures as other groups but the common carotid arteries were not occluded; Group (2) control (ischemic-reperfused) group: the rats were subjected to the same surgical procedures as other groups with bilateral common carotid artery occlusion (BCCAO) for 30 min. followed by reperfusion for 1 hr but without drug; Group (3) control vehicle group: three days before surgery, rats received daily the vehicle of rosuvastatin drug, normal saline (0.9% Nacl) (1 ml/kg/day) intraperitoneally, then anesthesia and surgery with BCCAO for 30 min. followed by reperfusion for 1 hr were done and Group(4) rosuvastatin treated group: rats received daily rosuvastatin intraperitoneally. The dose of rosuvastatin was (10 mg/kg /day) for three days before the surgery, then anesthesia and surgery with BCCAO for 30 min. followed by reperfusion for 1 hr. Results: At the end of the experiment, the levels of cerebral TNF-α, IL-6, IL-10,Caspase- 3,Bax,MDA,CD4 and MPO significantly (p < 0.05) increased in control group as compared with the sham group and the level of cerebral GSH significantly (p < 0.05) decreased in control group as compared with the sham group, while there was insignificant difference in cerebral levels of CD8 between the four experimental groups. Histopothological analysis showed that rats in control group showed significant cerebral injury. Treatment with rosuvastatin significantly counteracted the increase in the cerebral levels of TNF-α, IL-6, IL-10,Caspase-3,Bax,MDA,CD4 and MPO and the decrease of GSH. Histopathological analysis revealed that rosuvastatin significantly (P < 0.05) reduced the severity of cerebral injury in the rats underwent BCCAO. Conclusions: The results of the study revealed that inflammatory cytokines, apoptosis pathways and oxidative stress mediators are involved in global cerebral ischemia induced by bilateral common carotid artery occlusion. Cerebral ischemia reperfusion injury can be modified by rosuvastatin via its anti-inflammatory, anti-apoptosis and anti-oxidant effects.
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