The Effects Of Thyroid Hormone On The Expression Of NF-κB And TNF-α After Cerebral Ischemia Reperfusion Injury In Rats

BackgroundIschemic cerebrovascular disease is a high incidence、high morbidity and high mortality tenors disease.It is a serious threat to the human health and it affect the quality of life.In recent years,the treatment of ischemic cerebrovascular disease mainly arteriovenous thrombolysis,mechanical thrombosis and so on.The main purpose is to timely recurrent blood flow,save the ischemic penumbra.After vascular recanalization,the tissue cells obtain fresh blood flow,thus avoid further ischemia and hypoxia,but with the resulting ischemia and reperfusion injury problem is currently the most prominent and the study of popular issues.Ischemia reperfusion injury means that the tissues and organs are not improved after the blood flow is re obtained,but new injuries occur.Ischemia-reperfusion injury is a complex pathological process.Inflammatory response is one of the important pathologic mechanisms involved.Which eventually leads to death of neuronal damage.Inflammatory cytokines NF-κB(nuclear factor-kappa B)and TNF-α(tumor necrosis factor)are expressed easily after cerebral ischemia.It can better simulate the pathophysiology of cerebral ischemia in the human body that take the cytokines NF-κB and TNF-α as an observation indicator.As we all know,thyroid hormone play an important role in the development of the central nervous system.There are few reports on thyroid hormones in ischemia-reperfusion injury.In this study,we developed rat model of ischemia-reperfusion injury.We observed the effects of thyroid hormone on the expression of inflammatory cytokines NF-κB and TNF-α.The role of thyroid hormone in the pathogenesis of inflammation is discussed,which provides a new idea for the treatment of cerebrovascular disease.ObjectiveTo explore the effects of Thyroid Hormone(T3)on the expression of NF-κB and TNF-α after cerebral ischemia-reperfusion injury in rats.MethodNinty-six healthy male SD rats were randomly divided into sham operation group,sham operation + T3 group,IR group,IR + T3 group.Using suture legal method to make a rat model of middle cerebral artery occlusion for 2h followed by reperfusion.T3 was given 6 h after reperfusion at 1 h after modeling,respectively,intraperitoneal injection T3 l0ug/100 g for rats.Rats in other groups were given at the same time ip with normal saline.Nerve function score was evaluated by Longa 5.The infarct size was determined by TTC staining at 24 h after the 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-κBmRNA 、TNF-α mRNA and its protein in ischemic cortex of rats.Result1.The neurological function score and percentage of cerebral infarction area in IR + T3 group were significantly lower than those in IR group(P<0.05).2.HE staining showed that the pathological damage of IR + T3 group was less than that of IR group.3.Real-time PCR and immunohistochemical results showed that there was no significant difference in the expression of NF-κB mRNA,TNF-α mRNA and protein in ischemic cortex of sham operation group and sham operation + T3 group.Compared with the sham group,the expression of NF-κB mRNA,TNF-α mRNA and protein in ischemic cortex of IR group were significantly increased(P <0.05).Compared with IR group,the expression of NF-κB mRNA,TNF-α mRNA and protein in IR + T3 group decrease(P<0.05).Conclusion1.Thyroid hormone has protective effect on cerebral ischemia-reperfusion injury in rats.2.The protective effect of thyroid hormone on ischemia-reperfusion injury is achieved by down-regulating the expression of inflammatory cytokines NF-κB and TNF-α.