| Objective:To study the expression of HSP22and P-Akt in brain contex following cerebral ischemia/reperfusion and intervention of atorvastatin in SD rats, and to probe the possible role of HSP22and P-Akt in cerebral ischemia/reperfusion and the possible protective mechanism of atorvastatin intervention.Methods:Models of cerebral ischemia/reperfusion in SD rats were established by middle cerebral artery occlusion (MCAO) for2hours followed by reperfusion72h.52SD male rats were randomly divided into four groups: normal group, sham operation group, cerebral ischemia/reperfusion group and intervention group. Nothing was done in former two groups; in cerebral ischemia reperfusion group,we administrated stomach with physiological saline only; but in intervention group, atorvastatin (lOmg/kg) was prepared with physiological saline according to reperfusion time (time of palinesthesia,24h and48h). All rats were executed after72h reperfusion. The brains were preserved with different methods for TTC staining, HE staining and TUNEL staining; the protein expression of HSP22, Akt, P-Akt and Caspase3in each group was investigated by Western blotting. Results of data were analyzed by statistic soft package of Spss17.0.Results:1. After cerebral ischemia/reperfusion, the volume of cerebral infarction(%) in intervention group was significantly diminution than those in cerebral ischemia-reperfusion group with TTC staining of brain tissue (16.72±3.63%vs.23.83±2.53%).2. After cerebral ischemia reperfusion, only few positive apoptotic cell were found in normal group and sham operation group with TUNEL staining (1.00±0.76vs.1.1±0.83). In cerebral ischemia reperfusion group, the positive apoptotic cell showing brownness with high power lens was scattered in ischemia semidarkness band, distributed not well, or concentrated in some area. The counts of apoptotic cell in cerebral ischemia reperfusion group was obviously higher than those in normal group or sham operation group (P<0.001); but in intervention group, the apoptotic cell was reduced significantly compared with cerebral ischemia/reperfusion group (25.13±3.18vs.43.88±4.12, P<0.001).3. After cerebral ischemia/reperfusion, comparing of normal group and sham operation group, we fond that low level of HSP22and P-Akt and lower level of Caspase-3were expressed in pallium of SD Rats (0.43±0.07vs.0.45±0.10,0.66±0.04vs.0.68±0.05,0.17±0.02vs.0.19± 0.04; P>0.05). In cerebral ischemia/reperfusion group, levels of HSP22, P-Akt and Caspase-3were evidently increased (1.76±0.13vs.1.67±0.10vs.0.64±0.04) when compared with normal group or sham operation group. In intervention group, the expression of HSP22and Caspase-3were reduced (1.06±0.19vs.0.34±0.08, P<0.001), but levels of P-Akt was significantly higher (2.14±0.27) than those in cerebral ischemia-reperfusion group (P<0.001).Conclusion:1. As a reaction to cerebral ischemia stress, signal pathway axis of HSP22/P-Akt/Caspase-3may be one of endogenous mechanisms of autoprotection following cerebral ischemia/reperfusion injury of SD rats.2. Atorvastatin may have an effect on originate component of heat shock stress reaction and relieve the stress reaction of cerebral ischemia, meanwhile decrease the levels of HSP22.3. Atorvastatin can promote the expression of P-Akt after stress reaction of cerebral ischemia/reperfusion, PI3K/Akt signal pathway may be one of the mechanisms to protect brain tissue from cerebral ischemia/reperfusion injury.4. Atorvastatin can decrease the expression of Caspase-3after stress reaction of cerebral ischemia and inhibit apoptosis of nerve cells in pallium.. |
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