| Objective: Performed focal cerebral ischemia reperfusion on the hyperlipidemia rats,this is to observe dynamic expression of brain ischemia side of STAT-3,IL-6 and apoptosis cells after ischemic postconditioning and to discuss the effect and its possible mechanism of ischemic postconditioning to the cerebral ischemia reperfusion injury in hyperlipidemia rats.Methods: 115 SD rats were randomly divided into two groups,one group with normal feed(10),another group of feeding high fat forage(105),in 28 days later,hollow heart blood tested in two groups of rats serum lipid indicators,respectively,serum total cholesterol(TC),triglyceride(TG),low density lipoprotein(LDL-C),high density lipoprotein(HDL-C),and compared two sets of content,if there were significant differences(P < 0.05),indicating that hyperlipidemia rats building success.Hyperlipidemia rats randomly divided into sham group(35),ischemia reperfusion group called I/R group(35),ischemic postconditioning group called IP group(35).The animal models of I/R group and IP group were made by using the method of improved line plug and gave reperfusion in 2 hour,postoperative 30 rats could be divided into six groups averagely according to the different time points,each time point set were 3 h,6 h,12 h,24 h,48 h,72 h,IP group gave 15 s ischemia reperfusion before giving infusion 15 s,three loop repeatedly before giving reperfusion,sham group only seamed incisions after separation ofcarotid artery.Among them,the sham group used 5 rats brain tissue to take the TTC staining in 24 hours after the operation,IP and I/R group used 5 rats brain tissue to take the TTC stainin in 24 hours after the reperfusion,and calculated infarction volume by the TTC staining.Through the neural function defect scale judged the neurologic deficits at each time point,HE staining observed the pathological changes of cerebral infarction group in different time points,Tunel method detected the number of nerve cell apoptosis,immunohistochemical method(Envision)detected the expression of STAT-3and IL-6.Result : 1.The hyperlipidemia rats model : a high-fat feed group rats serum TC?TG?LDL – C?HDL-C content is significantly higher than the ordinary feed group(P < 0.05);2.The neural function defect scale: Sham group rats had no obvious neurologic deficits symptoms,I/R group appeared different degree of nerve dysfunction at different time points,lowest score in 24 hours,the difference was statistically significant compared with other time points,the IP group' s nerve function score was significantly higher than the same point in time reperfusion group after 12 hours in point(P <0.05);3.calculated cerebral infarction volume by TTC staining: the TTC staining of sham group's brain tissue at 24 hours after reperfusion were uniform red,brain tissue morphology were normal and no obvious pallor and edema;I/R and IP goup's line bolt lateral brain tissue at 24 hours after reperfusion were observed pale color,volume were greater than the wireless side brain tissue,and the I/R group's infarct area were bigger thanthe IP group(P < 0.05);4.Number of nerve cell apoptosis and the expression of IL-6 and STAT-3 immune positive cells: sham group not seen STAT-3 immune positive cells in brain tissue after immunohistochemical staining in the microscopic,and had little in leaves in IL-6.The expression of STAT-3 in I/R group appeared at 3h and peaked at 24 h,then started to reduce gradually at a later point-in-time,but had high expression at 72 h.The expression of IL-6 in I/R group had more positive expression than sham group at 3h and peaked at24 h,then started to reduce gradually at a later point-in-time,but had high expression at 72 h.IP group had similar variation trend,but quantity expression significantly reduced in same time point.Apoptotic cells and the expression of IL-6 and STAT-3 had similar variation trend.Conclusion: 1.On the basis of stablishing hyperlipidemia rat model made one side of middle cerebral artery cerebral infarction reperfusion model could better simulate the human brain infarction disease patterns,the indicators detected had more persuasive;2.After cerebral ischemia reperfusion rats appeared damage in behavior and morphology,and made IL-6,apoptotic cells and expression of STAT-3increased;3.The brain protective mechanisms of ischemic postconditioning could be inhibit the expression of IL-6,thereby reduced JAK2 / STAT3 pathway activation and the degree of apoptosis. |
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