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通过建立具有亚临床特点的实验性甲亢和甲低模型,对甲状腺功能状态改变影响药代动力学的机制从生化及细胞形态学水平上进行了初步的探讨.实验结果表明:甲状腺功能提高时,SD大鼠的相对肝重、肝微粒体蛋白含量及肝微粒体细胞色素P—450含量均较对照组分别增加22.10％、24.74％及42.42％.而甲低时则分别减少12.27％,14.95％及47.87％.通过对大鼠肝微’粒体进行SDS—聚丙烯酰胺凝胶电泳研究表明:甲状腺功能提高使分子量为17.5～94KD的大鼠肝微粒体P—450蛋白含量增加,甲状腺功能降低则减少.电镜观察表明,甲状腺功能提高时大鼠肝细胞光滑内质网显著增生,表面积增大,扩张成池,而甲状腺功能降低则光滑内质网明显减少,有的甚至消失。
Through the establishment of a subclinical experimental hypothyroidism and hypothyroid model, the mechanism of pharmacokinetics affecting thyroid function changes was discussed from the aspects of biochemistry and cell morphology.Experimental results show that when thyroid function is improved, Compared with the control group, the relative liver weight, liver microsomal protein content and liver microsomal cytochrome P-450 content in SD rats increased by 22.10%, 24.74% and 42.42%, respectively, while those in the control group decreased by 12.27% and 14.95% And 47.87%, respectively.The results of SDS-polyacrylamide gel electrophoresis showed that the increase of thyroid function increased the content of P-450 protein in rat liver microsomes with a molecular weight of 17.5-94KD and decreased thyroid function The number of smooth endoplasmic reticulum was significantly increased, the area of smooth endoplasmic reticulum increased significantly, the surface area increased, and expanded into a pool, while the decrease of thyroid function was significantly reduced smooth smooth endoplasmic reticulum, and some even disappeared.