目的观察碘缺乏和碘过量对大鼠心肌肌球蛋白重链(MHC)基因表达的影响。方法Wistar大鼠随机分为低碘(u)组、适碘(NI)组、5、10、50、100倍高碘(5HI、10HI、50HI、100HI)组,饲养6个月。采用化学发光方法测定血中甲状腺激素(TH)水平,记录大鼠心电图,心脏指数,RT—PCR法检测心肌肌球蛋白重链α和β(α-MHC、B—MHC)mRNA的表达。结果与NI组相比.LI组血清TH水平降低(P〈0.01),心脏指数增大(t=2.973,P〈0.01).心肌细胞α-MHCmRNA表达量降低(t=4.382.P〈0.01),β—MHCmRNA表达量增高(t=5.843,P〈0.01)。各HI组血清TH水平较NI组有下降趋势,10HI、50HI、100HI组血清,IT2与NI组相比差异有统计学意义(t=4.901、4.838、2.406,P〈0.01或0.05),10HI、50HI组血清TT4与NI组相比差异有统计学意义(t=2.162、2.348,P〈0.05);但心电图各波段和心脏指数未见明显改变;α-MHCmRNA表达量随摄入含碘量的升高而呈下调趋势,但与NI组相比差异无统计学意义(P〉0.05),而50HI和100HI组β—MHCmRNA表达量显著上调(t=2.632、4.127,P〈0.05或0.01)。结论碘缺乏和碘过量均可导致Wistar大鼠甲状腺功能减退(甲减),影响心脏受TH调节的靶基因的表达量,进而影响心脏的功能状态。
Objective To observe the effects of iodine deficiency and iodine excess on the expression of rat myocardial myosin heavy-chain (MHC) mRNAs. Methods 90 Wistar rats were divided into six groups: low iodine (LI), normal iodine (NI), five-fold iodine (5HI), ten-fold iodine (10HI), fifty-fold iodine (50HI) and one hundred iodine group (100HI) respectively and fed with water contained a series of concentration of KIOs. Six months after iodine administration, the level of thyroid hormone (TH) in serum was measured by'means of chemoluminescence. The electrocardiogram (ECG) and the heart weight to body weight ratio (H/B ratio) were recorded. Myocardial MHC mRNAs were detected by RT-PCR. Results As compared with NI groups, the level of serum TH (P 〈 0.01 ) was decreased whereas H/B ratio was increased with lower iodine treatment (t = 2.973 ,P 〈 0.01 ). The expression of α-MHC was significantly reduced (t = 4.382,P 〈 0.01 ) but the expression of β-MHC was marked enhanced by lower iodine treatment (t = 5.843,P 〈 0.01 ). In response to various iodine treatment, although the level of serum TH was not significantly changed in either iodine treatment: groups, there was a strong decreasing trend of serum TH among higher iodine treatment groups. The level of TY3 reduced by 10HI, 50HI and 100HI iodine treatment (t = 4.901,4.838,2.406 ,P 〈 0.01 ,P 〈 0.01 and P 〈 0.05 respectively), while the level of TT4 reduced by only 10HI and 50HI iodine treatment(t = 2.162,2.348,P 〈 0.05). In addition, wave patterns, intervals of ECG and H/B ratio was not significantly different among the groups (P 〉 0.05). The expression of α-MHC decreased along with the increase of iodine concentrations, but no significant difference was seen compared with NI group. Whereas, the expression of β-MHC in both 50HI and 100HI groups was higher than that in NI group (t = 2.632, 4.127, P 〈 0.05 or 0.01 ). Conclusions Iodine deficiency and iodine excess could induce h