甲状腺功能减退症的雌性大鼠心肌损伤时凋亡心肌细胞的表达

目的观察甲状腺功能减退症大鼠心肌损伤时雌激素在心肌细胞凋亡中的作用，进一步探讨甲状腺功能减退症心肌损伤的发生机制和影响因素。方法用丙基硫氧嘧啶连续灌胃制作甲状腺功能减退症大鼠模型。应用免疫组化技术及末端脱氧核苷酸转移酶介导的缺口末端标记法（TUNEL）分别动态观察雄性大鼠组（40只）和雌性大鼠组（40只）的心肌细胞凋亡情况及Caspase-3、Bcl-2在心肌细胞中的表达。结果甲状腺功能减退症大鼠出现心肌细胞凋亡，并且随着病程进展凋亡心肌细胞逐渐增多（P〈0．05）（雌鼠组3、6、8、10、12周凋亡心肌细胞平均个数依次为16．40±2．62、29．50±2．67、34．50±3．34、42．70±3．24、56．00±2．90，P〈0．05；雄鼠组3、6、8、10、12周凋亡心肌细胞平均个数依次为21．60±2．67、35．50±2．94、41．70±2．96、46．70±3．1I、60．70±3．31，P〈0．05），雌激素发挥了抗凋亡的作用。结论甲状腺功能减退症时心肌损伤与心肌细胞凋亡密切相关，在凋亡过程中除甲状腺激素参与调控细胞凋亡外，雌激素对于心肌细胞凋亡亦有所影响。

The myocardial apoptosis induced by myocardial cell injury in female rat model with hypothyroidism

Objective To study the effect of estrogen on myocardial injury in hypothyroidism rats and to reveal the pathology of occurrence and development of the myocardial injury in hypothyroidism rats. Methods The model of hypothyroidism rats was established by feeding propylthiouracil. The pathology of the female group （ n = 40） and male group （ n = 40 ） was observed dynamicly. The presence of myocardial apoptosis cell was demonstrated by the method of terminal deoxynucleotidyl transferase mediated dTUP nick end labeling （TUNEL）. And the immunohistochemistry was used to determine the expression of Caspase-3 and Bcl-2 in the myocardial cells. Results The myocardial cell apoptosis appeared in hypothyroidism rats. With the development of the disease, the apoptosis myocardial cell was increased progressively （Female rats group： the numbers of myocardial cell apoptosis at 3,6,8,10, and 12 weeks were 16.40 ± 2.62,29.50 ± 2. 67,34. 50 ± 3.34,42.70 ±3.24, and 56. 00±2. 90 respectively, P 〈 O. 05 ; Male rats group ： the numbers of myocardial cell apoptosis at 3, 6,8,10,and 12 week were 21.60 ±2.67,35.50 ±2.94,41.70±2.96,46.70 ±3. 11,and 60.70±3.31 respectively, P 〈 0. 05 ）, which indicated that estrogen may be related to myocardial cell apoptosis. Concision The myocardial eell apoptosis is related with the myocardial injury in hypothyroidism rats. Myocardial cell apoptosis may result in the myocardial injury. The estrogen participates in regulating apoptosis, but its function gradually weakens with the development of the hypothyroidism.