HspB8 expression in brain tissue after cerebral ischemic reperfusion and atorvastatin intervention in Sprague–Dawley rats

OBJECTIVE: The aim of this study was to evaluate the expression of HspB8 in the brain cortex of Sprague-Dawley rats after cerebral ischemic reperfusion (I/R) and atorvastatin intervention. It also aimed to determine the possible mechanism of atorvastatin intervention. A model of cerebral I/R in Sprague-Dawley rats was used. METHODS: Fifty-two male Sprague-Dawley rats were randomly divided into four groups. The normal and sham-operated groups received no treatment. The I/R group was intragastrically administered with physiological saline, and the intervention group received atorvastatin (10 mg/kg) prepared with physiological saline according to reperfusion time (time of palinesthesia, 24 and 48 hours). All rats were killed after 72 hours of reperfusion. RESULTS: 2,3,5-Triphenyltetrazolium chloride staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling showed that atorvastatin significantly reduced the volume of cerebral infarction (%) in the brain tissue and attenuated neuronal apoptosis in the cortex of rats, respectively. HspB8 was expressed in the pallium of Sprague-Dawley rats in the normal and sham-operated groups. The expression level of HspB8 was significantly upregulated after cerebral I/R. However, the level of HspB8 expressed was lower in the intervention group than in the I/R group. CONCLUSION: The expression of HspB8 was upregulated after cerebral I/R injury. Atorvastatin affected the precursors of the heat shock stress response, relieved stress injury due to cerebral ischemia, downregulated HspB8 expression, and inhibited nerve cell apoptosis in the brain cortex. However, HspB8 might not contribute to atorvastatin-mediated cytoprotective effects.