Effect Of Minocycline On The Expression Of P-JNK,Bcl-2 And Neuron Apoptosis In The Rat Model Of Focal Cerebral Ischemia-referfusion

Objectives:To investigate the effect of minocycline(MC)on the histologic outcome,apoptosis and expression of p-JNK,Bcl-2 at different time points on the model of focal cerebral ischemia-reperfusion injury in rats.Methods:1.Focal cerebral ischemia-reperfusion model was established by the occlusion of right middle cerebral artery.2.72 Healthy male Wistar rats were randomly divided into sham group, ischemia-reperfusion(I-R)group,MC treated group,each 24.Each respectively in 1h after ischemia-reperfusion 6h,12h,24h,and 48h for detection.3.HE staining of pathological in brain tissue morphology;immunohistochemical methods to detect the P-jnk and Bcl-2 protein expression changes;TUNEL staining of the group to observe the neuronal apoptosis.Results:1.HE staining shows that infarction and neuronal injury was relieved at different time points in the MC treated group compared with I-R group.2.Immunohistochemical results show that:①Expression of p-JNK positive cells was found in ischemic cortex after cerebral ischemia followed by reperfusion,and gradually increased at 6h after referfusion,at 48h after referfusion reaching the top(P＜0.01).expression of p-JNK in minocycline treated group at all time points were significantly decreased.(P＜0.01).②There were elevated expression of Bcl-2 in I-R group compared with sham operation group,the level of positive expression varied to the duration of reperfusion,and reached the peak level at 12h reperfusion after 1h cerebral ischemia(P＜0.01).expression of Bcl-2 in minocycline treated group at all time points were significantly increased(P＜0.01).3.A large number of TUNEL-positive cells were observed in I-R group,the number of apoptotic cells was higher than that of sham-operated group(P＜0.01).TUNEL positive cells of cerebral cortex and striatum were markly reduced in MC treated group(P＜0.01).Conclusions:1.The rats development typical symptoms of neurological impairment.TTC staining showed infarction.Cerebral HE staining results in line with pathological process.2.The protein expression of p-JNK and Bcl-2 participated in the occurance of ischemic cellular injury,including apopoptosis. 3.Minocycline obviously inhibited transient focal cerebral ischemia induced apoptosis in cortex and striatum,up-regulate the expression of Bcl-2 and downregulate p-JNK.Minocycline could attenuate cell death after cerebral ischemia-referfusion,show a neuroprotective effect.