| Objective:To study the effects of Rosuvastatin on neuronal deficitsand the expression of STAT3,JAK2and TNF-α after focal cerebralischemia/reperfusion in Rats,and the possible mechanism of Rosuvastatin for itscerebral protection.Methods:Prepared hyperlipidaemia rats model.Prepared130male rats,and randomly selected10as the normal group which were feed withnormal fodders,and the left120were feed with high-fat fodders.After fourweeks feeding,checked the total cholesterol,triglyceride,low density lipoproteincholesterin and high density lipoprotein cholesterin.The differences betweentwo groups had statistics,which showed the hyperlipidaemia model wassucceed.The hyperlipidaemia rats were randomly divided to four groups,thesham-operated group,the cerebral ischemia-reperfusion group,the low-doseRosuvastatin treatment group and the high-dose Rosuvastatin treatmentgroup,each group contented30rats.Gave gavage the sham-operated group andthe cerebral ischemia/reperfusion group once a day with sterile distilled water1.0mL/100g,the low-dose Rosuvastatin treatment group with0.5mg/kgrosuvastatin dissolved inside,and the high-dose Rosuvastatin treatment groupwith4.0mg/kg rosuvastatin dissolved inside.After continuous medication fortwo weeks,ligatured right middle cerebral artery of all rats except thesham-operated group to build cerebral ischemia/reperfusion model.Each groupwas observed at5time point which were2h,6h,12h,24h,72after the operation.And the each time point of24h,and every5rats were done TTC staining andmeasure the volume of cerebral infraction.At different time point,using thedry-wet weight method to detect water content of brain tissue.Observed theneuronal deficits and judged whether the model was succeed by the neurological dysfunction scores.Observed the cerebral infarction tissuepathological change at different time by HE staining section.Checked thedynamic change of the expression of STAT3,JAK2and TNF-α byimmunohistochemistry methods.Result:1.The neurological dysfunction scores:The sham-operated group had no neuronal deficits.The cerebral ischemia-reperfusion group,the low-dose Rosuvastatin treatment group and thehigh-dose Rosuvastatin treatment group had respective neuronal deficits,butscores of the Rosuvastatin treatment groups were higher than those of thecerebral ischemia/reperfusion group(P<0.05),and scores of the high-doseRosuvastatin treatment group were higher than the low-dose Rosuvastatintreatment group(P<0.05).2.The expression of STAT3and JAK2:Theexpressions of JAK2STAT3in the sham-operated group were rare absent.Twohours after ischemia-reperfusion,JAK2and STAT3could be detected inischemic part of the cerebral ischemia-reperfusion group,the low-doseRosuvastatin treatment group and the high-dose Rosuvastatin treatment groupand they reached the peak at the time point of24hours after reperfusion andreduced72hours after reperfusion.The expressions of JAK2and STAT3inRosuvastatin treatment groups were fewer than those of the cerebralischemia/reperfusion group(P<0.05),and the expression in the high-doseRosuvastatin treatment group were fewer than the low-dose Rosuvastatintreatment group(P<0.05)3.The expression of TNF-α:The TNF-α cells in thesham-operated group were rare observed.But it could be clearly observed inischemic part of the cerebral ischemia/reperfusion group,the low-doseRosuvastatin treatment group and the high-dose Rosuvastatin treatment groupat the time point of2hours after reperfusion then it increased and reached thepeak at the time point of24hours after reperfusion and reduced72hours afterreperfusion.And the expression of TNF-α were significantly higher thansham-operated group(P<0.01).The expressions of TNF-αin Rosuvastatintreatment groups were lfewer than those of the cerebral ischemia/reperfusion group(P<0.05),and the expression in the high-dose Rosuvastatin treatmentgroup were fewer than the low-dose Rosuvastatin treatment group (P<0.05).Conclusion:1.The hyperlipidaemia rats had neuronal deficits, brain edema andbrain ischemia after cerebral ischemia/reperfusion.2.The expression of JAK2,STAT3,TNF-α increased after cerebral ischemia-reperfusion,and this may act arole in the its pathophysiologic process.3.Rosuvastatin could be a potentneuro-protector by inhibiting the neuronal deficits and the signal pathwayinvolving the JAK2/STAT3to reduce the amount of apoptotic cells. |
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