摘要
目的观察甲状腺功能减退症大鼠心肌损伤时Caspase-3和Bc l-2在心肌细胞中的表达,探讨甲减心肌损伤的发生机制以及与甲状腺功能的关系,及给予左甲状腺素钠(优甲乐,L-T4)进行干预治疗后的影响。方法用丙基硫氧嘧啶(PTU)连续灌胃制作甲状腺功能减退症大鼠模型。分别动态观察对照组、甲减组和干预组大鼠的心肌病理改变及损伤情况,并同时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)检测Caspase-3和Bc l-2在心肌细胞中的表达及心肌细胞凋亡情况。结果甲减大鼠出现心肌细胞凋亡,并且随着病程进展凋亡逐渐加重,并与甲状腺功能密切相关。优甲乐干预后细胞凋亡明显减少。结论甲减时心肌损伤与心肌细胞凋亡密切相关,即心肌细胞凋亡可引起甲减心肌损伤,给予优甲乐干预后细胞凋亡减少,心肌损伤减轻。
OBJECTIVE To study the expression of the effeeter molecule of myocardial cell apoptosis （Caspase-3） and the resisting apoptosis protein （ Bel-2 ） in hypothyroidism rats revealed the pathology of occurrence and development of the myocardial injury in hypothyroidism, and effects of LT4 intervention. METHODS The model of hypothyroidism rats was made by giving them propyhhiouracil. The pathology condition of the control group and hypothyroidism group 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 was aggravated progressively, which was related with the thyroid function. The myocardial cell apoptosis had reduced after LT4 intervention. CONCLUSION The myocardial cell apoptosis was related with the myocardial injury in hypothyroidism rats. It was said that the myocardial cell apoptosis resulted in the myocardial injury. The thyroid hormone participated in regulating apoptosis.
出处
《中国现代应用药学》
CAS
CSCD
北大核心
2008年第6期482-487,共6页
Chinese Journal of Modern Applied Pharmacy
基金
河北省科技厅科技攻关项目(项目编号:06276102D-106)
