| Objective The cerebrovascular accident rate in China is as high as 1.5-2.0 ‰.Ischemic cerebrovascular disease has become the highest morbidity and mortality of the disease.Timely recovery of brain tissue blood supply is the best way to save the lives of patients with cerebral ischemia,but to restore blood flow after the brain tissue brings a new damage,that is,ischemia and reperfusion injury.How to reduce the reperfusion injury has become one of the hotspots of medical research.In order to investigate the effect of thyroid hormone on cerebral ischemia-reperfusion injury in rats,and to observe the rats neurological functional score,the changes of infarct volume,pathological changes,cytochrome C(Cyt C)and apoptosis inducing factor(AIF)which these two kinds of pro-apoptotic-related factors in the ischemic penumbra expression changes to study its possible mechanism.Methods SD rats were randomly divided into 4 groups :sham group(Sham1),sham + T3 group(Sham2),ischemia-reperfusion group(IR),IR + T3 group(T3).each group of 24,the right MCAO model was established according to the reforming Zea-Longa suture-occluded method,sham operation group received similar treatment but did not accept the insertion of the line embolism,IR group and T3 group inserted after the bolt 2h pull out the line embolism.Sham2 group and T3 group were given intraperitoneal injection of thyroid hormone 10 ug / 100 g at 1h postoperatively and 6h after infusion,the other two groups were injected with saline as placebo.The neurological function score was performed 24 hours after reperfusion,then the rats were killed,Eight rats in each group were subjected to TTC staining and then the percentage of cerebral infarction volume was measured,another 8 rats were treated with cerebral perfusion fixation,then the brain tissue was taken and then HE staining was performed to observe the pathological changes,the positive expression of Cyt C and AIF cells in ischemic penumbra was observed by immunohistochemistry.The expression of Cyt C and AIF m RNA was detected by real-time quantitative PCR in the last 8 rats.Results 1.From the neurological deficit score,the percentage of cerebral infarction volume,and the pathological changes of the brain tissue to observe: Sham1 and sham2 had no neurological deficit,ischemic infarction,and histopathological changes;Compared with IR group,the score of neurological deficit in group T3,the percentage of cerebral infarct volume decreased,and the pathological changes of infarct brain were reduced(P <0.05);2.Immunohistochemical method for the expression of Cyt C and AIF cells: sham1,sham2 group of ischemic penumbra region occasionally Cyt C and AIF positive cells,IR group showed a large number of Cyt C and AIF positive cells in this region,Compared with IR group,the expression of Cyt C and AIF positive cells in T3 group was significantly decreased(P <0.05);3.3.Real-time quantitative PCR analysis of Cyt C and AIF m RNA levels: The level of Cyt C and AIF m RNA in ischemia-reperfusion group was significantly higher than that in sham1 operation group and sham2 operation group;The level of Cyt C and AIF m RNA in rats treated with T3 was significantly lower than that in ischemia-reperfusion rats.(P < 0.05)Conclusions 1.Thyroid hormone T3 can significantly improve the ischemia reperfusion injury of rat neural dysfunction,reduce the percentage of infarct volume,and improve pathological change,indicating that T3 on cerebral ischemia-reperfusion injury in rats with neuroprotective and repair effect.Ischemic penumbra Cyt C,AIF positive expression cells decreased,Cyt C,AIF m RNA levels decreased,and decreased apoptosis,which play a protective role of the brain;2.Thyroid hormone on the ischemic foci around the cortical area which cerebral ischemia-reperfusion injury in rats has a protective effect,The mechanism may be related to the inhibition of apoptosis factor Cyt C and AIF expression to further inhibit mitochondrial apoptosis pathway. |
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