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目的探讨母源性甲状腺功能亢进(简称甲亢)对新生仔鼠心脏中甲状腺激素受体的影响。方法首先对24只雌性Wistar大鼠建立妊娠合并甲亢模型,取新生5d、10d、15d仔鼠心脏进行解剖检查,取部分心脏组织石蜡切片Masson染色,取部分心脏组织采用实时定量PCR法检测甲状腺激素受体(TR)α1、TRα2、TRβ1mRNA水平表达量的变化。结果在心脏组织中TRα1mRNA的表达量较TRα2、TRβ1的表达量高,且在出生10d的仔鼠心脏(包括甲亢组和对照组)中TRα1mRNA的表达量呈现峰值;与同期对照仔鼠相比,母源性甲亢仔鼠出生5d与出生10d心肌中TRα1mRNA的表达量显著上调,出生15d的表达量与对照组相比表达量下调;TRα2在母源性甲亢和对照中差异无统计学意义;TRβ1在甲亢出生5d仔鼠中表达量显著下调,10d组表达量上调,15d组表达量差异无显著性。结论母源性甲亢会对仔鼠心肌产生影响,引起甲状腺激素受体的差异表达;这种变化随出生后时间延长而减弱。甲状腺激素受体中TRα1的变化最显著,可能在甲亢引起的心肌损伤中起重要作用。
Objective To investigate the effect of maternal hyperthyroidism (Hyperthyroidism) on thyroid hormone receptors in the heart of neonatal offspring. Methods Thirty-four female Wistar rats were used to establish pregnancy-associated hyperthyroidism model. The hearts of neonatal 5d, 10d and 15d neonates were dissected. Masson staining of some heart tissues was performed. Some cardiac tissues were collected for detection of thyroid hormone (TR) α1, TRα2, TRβ1 mRNA expression level changes. Results The expression of TRα1 mRNA in heart tissues was higher than that of TRα2 and TRβ1, and the expression of TRα1 mRNA in the offspring hearts of 10-day-old rats (including hyperthyroidism group and control group) showed the peak value. Compared with the control group, The expression of TRα1 mRNA in maternal hyperthyroidism offspring was significantly increased at 5 days of birth and at 10 days of birth, and the expression of TRα1 at 15 days after birth was down-regulated compared with that of the control group. There was no significant difference of TRα2 between maternal hyperthyroidism and controls. TRβ1 The expression of 5-day-old offspring of hyperthyroidism was significantly down-regulated, while the expression of 10-day group was up-regulated. There was no significant difference in 15d group. Conclusion Maternal hyperthyroidism exerts an influence on the myocardium of the offspring, which causes the differential expression of thyroid hormone receptors. This change is weakened with the prolongation of postnatal period. The most significant change of TRα1 in thyroid hormone receptor may play an important role in myocardial injury caused by hyperthyroidism.