高碘对大鼠甲状腺过氧化物酶和钠碘转运体基因mRNA表达的影响

目的 观察长期碘过量对大鼠甲状腺过氧化物酶(TPO)和钠碘转运体(NIS)mRNA表达的影响.方法 将SD大鼠按体质量随机分为对照(CI)组、高碘Ⅰ(HI Ⅰ)组、高碘Ⅱ(HIⅡ)组,分别饮用含碘5、5000、10000μg/L的自来水.6个月时取大鼠甲状腺,在光、电镜下观察甲状腺形态结构的变化;采用放射免疫法测定血清甲状腺激素水平;RT-PCR法检测甲状腺TPO、NIS mRNA的表达.结果 高碘组与CI组相比.部分甲状腺滤泡明显增大,滤泡腔内充满浓染胶质;血清TT4 、TT3水平,HI Ⅰ组[(73.82±16.48)、(1.34±0.31)nmol/L]和HIⅡ组[(70.65±11.43)、(1.15±0.39)nmol/L]与对照组[(75.68±13.99)、(1.45±0.49)nmol/L]相比呈逐渐下降趋势,但组间差异无统计学意义(F值分别为0.371、1.163,P＞0.05);TPO、NIS mRNA表达水平,组间比较差异有统计学意义(F值分别为30.863、62.675,P＜0.05).HI Ⅰ组(1.28±0.10、0.56±0.17)和HIⅡ组(1.14±0.04、0.39±0.06)均比对照组(1.39±0.08、0.71±0.13)明显降低(P＜0.05).结论 长期碘过量可造成甲状腺组织形态学改变,并且抑制甲状腺TPO、NIS mRNA表达.

Effects of iodine excess on TPO and NIS genes mRNA expression in rats

Objective To observe the effects of iodine excess on thyroid morphology,the expression of thyroid peroxidase and sodium iodide symporter mRNA and to explore their mechanisms.Methods One-month SD rats were divided into three groups:control iodine(CI),high iodine Ⅰ(HI Ⅰ)and high iodineⅡ(HI Ⅱ)and were fed with water containing iodine in different concentrations by adding K103(5,5000,10 000μg/L)respectively.Rats were sacrificed after being fed for six months.The morphology of thyroid was investigated under light microscopy and electron microscopy,the serum thyroid hormones and ratio of TPO/β-actin and NIS/β-actin were measured by radio-immunoassay and RT-PCR method.Results The major changes were increased follicles with colloid accumulation in HI groups.The levels of serum thyroid hormones TT3 and TT4 were decreased gradually from CI[(75.68±13.99,1.45±0.49)nmol/L]to HI Ⅰ[(73.82±16.48,1.34±0.31)nmol/L]and HIⅡ groups[(70.65±11.43,1.15±0.39)nmol/L],but there were no significant differences among three groups(F=O.371,l.163,P＞0.05).The TPO and NIS mRNA expressions in HI Ⅰ(1.28±0.10,0.56±O.17)and HI Ⅱ(1.14±0.04,0.39±0.06)were significantly lower(F=30.863,62.62.675,P＜O.05)than those of control group(1.39±0.08,0.71±0.13).Conclusions Chronic iodine excess leads to definite histological changes in rat thyroid,and inhibits the expressions of TPO and NIS mRNA as well as thyroid hormone synthesis,which in turn acts as a protective mechanism against iodine excess.