探讨雷帕霉素对甲状腺炎大鼠氧化应激的改善作用OA

Objective To investigate the effect of rapamycin-induced oxidative stress on thyroiditis rats.Methods A rat model of thyroiditis was constructed and rapamycin was intervened.The levels of reactive oxygen species(ROS)and glutathione(GSH)in thyroid tissue of rats were detected by colorimetry.HE staining was used to observe the pathological morphology;the expression of chemokine receptor 3(CXCR3)and C-C chemokine receptor(CCR4)in thyroid tissue of rats was detected by PCR.The phosphorylation level of rapamycin target protein(mTOR)and the level of autophagy protein LC3-Ⅱ protein in thyroid tissue of rats were detected by immuno-histochemistry.Western blot was used to detect the expression of CXCR3,CCR4,Beclin-1 and LC3 protein in thyroid tissue of rats.Results Compared with the normal control group,the levels of ROS,CXCR3,CXCR3 mRNA expression and the number of p-mTOR positive cells in the thyroid tissue of the model group were increased(P<0.05),while the levels of GSH,CCR4,Beclin-1,LC3,CCR4 mRNA expression and the number of LC3-Ⅱ positive cells were decreased(P<0.05).Compared with the model group,the levels of ROS,CXCR3,CXCR3 m RNA expression and the number of p-mTOR positive cells in the dexamethasone group and the rapamycin group were decreased(P<0.05),and the rapamycin group was lower(P<0.05).The levels of GSH,CCR4,Beclin-1 and LC3,the expression of CCR4 mRNA and the number of LC3-Ⅱ positive cells increased(P<0.05),and the rapamycin group was higher(P<0.05).Conclusion Rapamycin can improve the level of oxidative stress,inhibit the expression of p-mTOR,increase the level of LC3-Ⅱ and autophagy in rats with thyroiditis,and regulate the expression of CXCR3/CCR4 protein.