Objective To investigate the effect of thyroid hormone(T3)on the expressions of cytochrome c (CytC) and apoptosis?inducing factor(AIF) after cerebral ischemia reperfusion injury in rats and its mechanism. Methods SD male rats were randomly divided into four groups: sham operation group(sham1),sham operation group + T3(sham2) ,ischemia?reperfusion group (IR) ,and thyroid hormone treatment group(T3). A rat model of cerebral ischemia?reperfusion injury was established by right middle cerebral artery occlusion for 2 h,followed by reperfusion for 24 h. Thyroid hormones (10μg/100 g) or normal saline were given at 1 h after onset of ischemia and 6 h after reperfusionby intraperitoneal injection. Neurological deficit scores were evaluated 24 h after reperfusion. Cerebral infarction volume was evaluated by TTC staining. Histological changes was observed by HE staining. Expressions and mRNA levels of CytC and AIF in ischemic brain tissue were evaluated by immunohistochemistry and real?time fluorescent quantitative RT?PCR. Results Ascompared with those in sham operation groups ,the expressions and mRNA levels of CytC and AIFincreased significantlyin IR groups. As compared with those in IR groups ,the indexes were remarkably decreasedin T3 groups (P < 0.01). Nerve function was markedly improved andinfarction area narrowed.Conclusions Thyroid hormone plays a certain role in protection of cerebral ischemia?reperfusion injury in rats,whose mechanism may be associated with inhibition of the expression of apoptosis factors?CytC and AIF.

Objective To investigate the effect of thyroid hormone on the expression of NF-κB and TNF-oα in the ischemic cortex of rats after focal cerebral ischemia-reperfusion.Methods 96 male SD rats were randomly divided into sham-operation group,sham-operation+T3 group,IR group and IR+T3 group.Using suture legal method to establish a rat model of middle cerebral artery occlusion for 2 h followed by reperfusion.In sham-operation+T3 group and IR+T3 group,T3 was given 3 days before ischemia and 1 hour after ischemia,respectively,intraperitoneal injection T3 10 μg/100 g for rats.Rats in other groups were given the same volume normal saline at the same time.The infarct size was determined by TTC staining at 24 h after reperfusion.HE staining was used to observe the morphological and structural changes of brain tissue.Using Real-time PCR method and immunohistochemical staining method to detect the expression of NF-κB mRNA,TNF-α mRNA and protein in ischemic cortex of rats.Results Compared with sham-operation group and sham-operation+T3 group,the pathological damage of brain tissue in IR group was obvious,while the pathologic damage of IR +T3 group was less than that in IR group.Immunohistochemistry assay showed that the expression of NF-κB was(49.19±5.55)in sham-operation group,(45.75±2.12) in sham-operation+T3 group,(56.88±2.23)in IR group and(50.25±1.67)in IR +T3 group,the expression of TNF-α was (22.50±3.07) in sham-operation group,(24.13±2.03) in sham-operation+T3 group,(37.25±2.82) in IR group and (30.25±1.67) in IR +T3 group,and the NF-κB,TNF-α in IR group were obviously higher than that in sham-operation group and sham-operation+T3 group(P＜0.05),while IR+T3 group were lower than that in IR group(P＜0.05).Real-time PCR showed that NF-κB mRNA,TNF-α mRNA level in IR group was the highest,which was higher than that of sham-operation group and sham-operation+T3 group(P＜0.05),and the NF-κB mRNA,TNF-oα mRNA expression in IR+T3 group were significantly decreased compared with that in IR group(P＜0.05).Conclusion Thyroid hormone has a protective effect on cerebral ischenia reperfusion injury,which may be achieved by reducing the expression of inflammatory factor NF-κB and TNF-oα.