【摘要】 目的探讨大鼠毒鼠强中毒的病理机制。方法SD大鼠60只,随机分正常对照组、空白对照组、高剂量中毒死亡组、低剂量中毒组,高剂量中毒死亡组以1.0mg/kg毒鼠强悬浊液灌胃,低剂量中毒组以0.1mg/kg体重毒鼠强悬浊液灌胃。用免疫组织化学技术对中毒大鼠器官检测caspase-3与Bcl-2蛋白的表达,用图像分析技术对检测结果进行分析。结果各器官caspase-3与Bcl-2蛋白的表达变化规律基本相似,即高剂量中毒组大鼠caspase-3与Bcl-2蛋白均呈较强的阳性表达,低剂量中毒组大鼠,Bcl-2与caspase-3于中毒30min后表达不明显,3h时,可见较为明显的阳性信号,Bcl-2在6h～3d达高峰,随后表达下降;caspase-3在24h～5d达峰值,随后下降。Bcl-2峰值早于caspase-3出现。结论Bcl-2与caspase-3参与了毒鼠强中毒的病理生理过程。更多还原

【Abstract】 Objective To find whether Bcl-2 and Caspase-3 take part in the pathophysiological mechanism of tetramine toxification. Methods Sixty Sprague-Dawley rats were divided into normal control group, the sham poisoned group, high dose poisoned group, low dose poisoned group.High dose poisoned group were administered 1.0 mg/kg weight body tetramine by mouth, however low dose poisoned group was administered tetramine 0.1 mg/kg weight body by mouth. The rats of the sham poisoned group were administered water, and rats of normal control group were given nothing. Bcl-2 and Caspase-3 were detected by immunohistochemistry staining and the results were assessed by image analysis system. Results The expressions of Bcl-2 and Caspase-3 in all organs were similar, ie, Bcl-2 and Caspase-3 expressed obviously in all organs of high dose poisoned group; in all organs of low dose poisoned group, they were hardly detected at 30 min after administration, however, at 3 h after administration, they could be detected obviously; Bcl-2 got to peak at 6 h～3 d after administration and Caspase-3 got to peak at 24 h～3 d after administration. Conclusion Bcl-2 and Caspase-3 take part in the pathophysiological procedure of tetramine poisoned rats.更多还原