不同碘摄入量对大鼠促甲状腺激素受体mRNA与钠碘转运体蛋白表达的影响

Impact of different doses of iodine intake on expressions of TSHR mRNA and NIS protein in rats

目的:观察不同碘摄入量对大鼠甲状腺组织中促甲状腺激素受体(TSHR)mRNA和钠碘转运体(NIS)蛋白表达的影响。方法:36只SD大鼠随机均分为低碘组、适碘组和高碘组。于实验第4,8周后分批处死大鼠,分别用实时荧光定量PCR和免疫组织化学法检测甲状腺组织中TSHR mRNA和NIS蛋白表达水平。结果:实验4周后,与适碘组比较,TSHR mRNA表达量在低碘组明显升高(P<0.05),而在高碘组略有降低,差异无统计学意义(P>0.05);NIS蛋白表达率在低碘组有所升高,高碘组有所降低,但差异均无统计学意义(均P>0.05)。实验8周后,与适碘组比较,低碘组和高碘组的TSHR mRNA和NIS蛋白表达水平均明显低于适碘组(均P<0.05),其中NIS蛋白表达率分别为同组4周后的44.03%和56.12%(均P<0.05)。结论:无论碘过量或碘缺乏,长期碘营养障碍均可降低NIS的表达,且该影响可能是通过TSH-TSHR信号通路活性改变所介导。

Objective：To observe the influence of different doses of iodine intake on the expressions of thyroid-stimulating hormone receptor（TSHR） mRNA and sodium/iodide symporter（NIS） protein in thyroid tissue of rats. Methods：Thirty-six SD rats were equally randomized into low iodine group,normal iodine group and high iodine group.Half of the number of rats of each group were sacrificed at the end of 4 and 8 weeks,respectively.The expressions of TSHR mRNA and NIS protein in the rats＇ thyroid tissues were determined by real-time PCR and immunohistochemical staining,respectively. Results：Compared with the normal iodine group at the end of 4 weeks of the experiment,the TSHR mRNA expression level in low iodine group significantly increased（P0.05）,and slightly decreased in high iodine group but the difference had no statistical significance（P0.05）;the NIS protein expression in low iodine group increased to some extend and somewhat decreased in high iodine group,but both differences reached no statistical significance（both P0.05）.Compared with the normal iodine group at the end of 8 weeks,the expressions of TSHR mRNA and NIS protein in both the low iodine and high iodine group were significantly reduced（both P0.05）,in which the NIS expression levels dropped to 44.03% and 56.12% of what they had reached at the end of 4 weeks,respectively（both P0.05）. Conclusion：In either iodine-excessive or iodine-deficient conditions,the long-term iodine disorder can decrease NIS expression,which is possibly mediated by the alterations of the TSH-TSHR signaling activity.