摘要目的 研究低碘膳食对大鼠脑组织同源盒基因nkx2.1表达的影响.方法 雌性Wistar大鼠40只,按体质量随机分为低碘组和对照组,均饲以含碘量为13.66μg/kg的低碘饲料,分别饮用去离子水和200μg/L碘酸钾溶液,3个月后用化学发光免疫分析方法测定大鼠血清甲状腺激素(Tr3、Tr4、FT3、FT4),再将两组大鼠与健康雄鼠进行交配,在孕16 d、新生及20日龄时,取胎鼠或仔鼠脑组织,用实时荧光定量PCR(FQ-PCR)法检测脑组织nkx2.1 mRNA表达.结果 大鼠血清TT3、TT4、FT3、FT4水平,低碘组[(0.89±0.20)、(0.32±0.16)nmol/L、(3.33±0.61)、(3.28±0.80)pmol/L]明显低于对照组[(1.04±0.06)、(39.42±14.68)nmol/L、(4.83±0.33)、(26.99±4.48)pmol/L;t值分别为2.71、6.52、5.70、12.89,P<0.05或<0.01].对照组孕16 d、新生及20日龄大鼠脑组织nkx2.1 mRNA表达分别为(5.60±0.30)×10-3、(1.20±0.29)×10-3、(0.18±0.06)× 10-3,低碘组同日龄大鼠nkx2.1 mRNA表达分别为(3.00±0.55)×10-3、(1.90±0.21)×10-3、(0.69±0.15)×10-3.对照组、低碘组各日龄胎、仔鼠之间nkx2.1 mRNA表达水平比较,差异有统计学意义(F值分别为2102.07、162.40,P均<0.01),对照组、低碘组新生仔鼠nkx2.1 mRNA的表达比孕16 d胎鼠低(P均<0.01),20日龄仔鼠nkx2.1mRNA表达比孕16 d和新生降低(P均<0.01);低碘组与同日龄对照组比较.对照组孕16 d胎鼠nkx2.1 mRNA表达明显高于低碘组胎鼠(t=16.073,P<0.01),而新生及20日低碘组明显高于对照组(t值分别为7.537、12.227,P均<0.01).结论 低碘导致的脑发育迟滞与nkx2.1在腩组织中的差异表达密切相关.

abstractsObjective To study the influence of low-iodine diet on the expression of homeobox gene nkx2.1 in rat cerebral tissue. Methods Forty female Wistar rats were randomly divided into two groups according to body. quality: low-iodine group and control group,both fed with low-iodine feed at an iodine content of 13.66 μg/kg,respectively given the deionized water and 200 μg/L KIO3 solution. The hormone levels of two group rats were determined with chemiluminescence immunoassay after three months, and then mated with healthy male rats. Cerebral tissues were taken from the fetus of 16-day pregnancy,newborn and 20 days old offspring in low-iodine and control group to detect the content of nkx2.1 mRNA using real-time fluorescence quantitative PCR (FQ-PCR) techniques. Results Serum TT3, TT4, FT3, FT4 level of rats in low-iodine group(0.89±0.20, 0.32±0.16, 3.33± 0.61, 3.28±0.80) was respectively lower than that in the control group(1.04±0.06, 39.42±14.68,4.83±0.33, 26.99±4.48;t = 2.71,6.52,5.70, 12.89, P < 0.05 or < 0.01). The relative nkx2.1 mRNA expression was(5.60± 0.30)×10-3, (1.20 ± 0.29)×10-3, (0.18± 0.06)×10-3 respectively in the fetus of 16-day pregnancy, newborn and 20 days old offspring of control group, while it was (3.00 ± 0.55)×10-3, (1.90 ± 0.21)×10-3,(0.69 ± 0.15)×10-3 in the low-iodine group. The difference of nkx2.1 mRNA expression was significant among fetal and neonatal rats in the control group and low-iodine group(F = 210.07,162.40, both P < 0.01). The nkx2.1 mRNA expression of newborn rats was lower than that of 16-day pregnancy in both groups(P < 0.01), and that of 20 days old rats was lower than that of 16-day pregnant and neonatal rats(P < 0.01). The 16-day pregnant rats of control group had obviously higher level of nkx2.1 expression than those in the low-iodine group(t = 16.073, P< 0.01), while the nkx2.1 of newborn and 20 days old low-iodine rats expressed much higher than healthy rats(t = 7.573,12.221, P < 0.01). Conclusions Brain development retardation caused by low-iodine is closely related to nkx2.1 differential expression in the brain tissue.