糖尿病大鼠甲状腺组织钠／碘转运体与促甲状腺激素受体mRNA及蛋白表达的变化

目的观察糖尿病大鼠甲状腺组织钠／碘转运体（NIS）、促甲状腺激素受体（TSHR）mRNA和蛋白表达的变化及氨基胍、胰岛素的干预作用，探讨高糖毒性致甲状腺组织损伤及其可能机制。方法高脂饲料喂养联合链脲佐菌素制备糖尿病大鼠49只，完全随机分为糖尿病组17只、氨基胍组16只，胰岛素组16只，设对照组9只，成模12周末称重并测血糖后处死，取甲状腺组织，以RT-PCR方法测定NIS、TSHRmRNA表达，Westem印迹方法检测NIS、TSHR蛋白表达。结果糖尿病组大鼠甲状腺组织NISmRNA和蛋白表达显著低于对照组（0．17±0．09VS0．47±0．16；0．42±0．28vs1．44±0．46；P〈0．05），TSHRmRNA和蛋白表达显著高于对照组（0．49±0．25vs0．17±0．18；1．48±0．65VS0．51±0．35；P〈0．05）；氨基胍组与胰岛素组糖尿病大鼠甲状腺组织TSHRmRNA和蛋白表达显著低于糖尿病组（0．29±0．28与0．30±0．15vs0．49±0．25；0．63±0．27与0．96±0．29vs1．48±0．65；P〈0．05），NISmRNA和蛋白表达显著高于糖尿病组（0．40±0．17与0．45±0．20vs0．17±0．09；0．76±0．36与0．75±0．28vs0．42±0．28；P〈0．05）。结论高糖毒性可能通过蛋白非酶糖基化途径致糖尿病大鼠甲状腺组织NIS表达下降、TSHR表达增高。

The changes of Sodium iodide symporter, thyrotropin receptor mRNA and protein expression in thyroid gland of diabetic rats

Objective To observe the changes of sodium iodide symporter (NIS), thyrotropin receptor (TSHR) mRNA and protein expression in diabetes mellitus(DM) rats as well as the intervention effects of aminogua-nidine and insulin, and to observe the damage effects of hyperglycemia toxicity on throid gland and the possible mechanisms. Methods Forty-nine rats were fed with high lipid feedstuff and intravenous injected with streptozocin to establish DM rat model and then were divided into DM group(n=17),aminoguanidine intervention group(n= 16) and insulin intervention group(n=16), meanwhile 9 rats were taken as controls. At the 12th weekend, rats were sacrificed and thyroid gland was taken to detect NIS and TSHRmRNA expression with RT-PCR skills and West-ern Blotting skills. Results NISmRNA and protein expression in thyroid glands of DM rats were much lower than those in NC group, while TSHRmRNA and protein expression were much higher than those in NC group(P<0.05). TSHRmRNA and protein expression after either aminoguanidine or insulin intervention were lower than those in DM group(P<0.05), but NISmRNA and protein expression were higher than those in DM group rats (P<0.05). Conclusion Hyperglycemia toxicity may lead to the decrease of NIS expression and increase of TSHR expression in thyroid gland of DM rats through protein nonenzymic glycation pathway.