内毒素休克大鼠血清TNF-α及心脏TNF-αⅠ型受体表达的变化及意义

Research on the changes of serum TNF-α and expression of TNF-α receptor type Ⅰ in the hearts of rats with endotoxic shock

目的 探讨肿瘤坏死因子-α（TNF-α）在内毒素休克时心脏损伤中的作用。方法 通过大鼠股静脉注射不同剂量内毒素建立内毒素休克动物模型，用ELISA方法检测不同时间点血清TNF-α水平，用免疫组化方法检测心脏TNF-αⅠ型受体的表达。结果注射内毒素后血清TNF-α水平开始上升，于90min达高峰，然后逐渐下降，于3．5h接近正常水平．而且小剂量组TNF-α上升幅度高于大剂量组。注射内毒素后TNF-αⅠ型受体表达明显增强，内毒素的剂量越大，TNF-αⅠ型受体表达越强。结论 内毒素休克时的心脏损伤与异常升高的TNF-α有关，TNF-α的负相肌力作用是通过诱导TNF-αⅠ型受体表达完成的，TNF-αⅠ型受体的异常表达为TNF-α发挥作用提供了信号转导基础。

Objective To investigate the changes of serum tumor necrosis factor α （TNF-α） and expression of TNF-α receptor type Ⅰ in the hearts of rats with endotoxic shock. Methods The animal model of endotoxic shock was established by injecting the different doses of endotoxin via femoral vein, and the serum TNF-α at different time pionts were detected by using ELISA; the TNF-α type Ⅰ receptor expression of the different groups were detected by immunohistochemical method. Results The level of TNF-α increased rapidly after endotoxin injecting, peaked at 90min, then decreased slowly, and recovered at 3.5 h. And the increase of TNF-α was greater in the group of small dose endotoxin then the group of large dose endotoxin. The expression of TNF-α type Ⅰ receptor was elevated and related to the dose of endotoxin. Conclusion The cardiac injury is caused by the elevated serum TNF-α, and the negative inotropic action of TNF-α is through inducing TNF-α type Ⅰ receptor overexpression of heart, which is promoted with the course of shock and related to the dose of endotoxin.