摘要
目的研究早期应用可溶性肿瘤坏死因子-α受体-IgG1 Fc段融合蛋白(sTNF-αR-Fc)对于感染性休克大鼠的治疗作用及可能的作用机制。方法30只Sprague-Daw ley大鼠随机平均分为对照组(注射生理盐水)、模型组(注射脂多糖)和sTNF-αR-Fc处理组(注射sTNF-αR-Fc和脂多糖)。多道生物信号分析系统监测各组大鼠平均动脉压变化并记录死亡情况;流式细胞仪检测脾细胞中TNF-α水平;RT-PCR检测肝脏及心脏组织TNF-α、IL-6 mRNA的表达水平。结果与对照组相比,模型组TNF-αmRNA表达水平升高,平均动脉压和生存率下降(P<0.05);与模型组相比,sTNF-αR-Fc处理组TNF-α、IL-6水平下降,生存率提高(P<0.05)。结论sTNF-αR-Fc可以显著降低脂多糖所致感染性休克大鼠的死亡率,其可能是通过降低TNF-α水平而起治疗作用。
To investigate the influence of soluble tumor necrosis factor-α receptor -IgG1 Fc fusion protein （sTNF-αR-Fc） on septic shock in rats and to understafid the underlying mechanism. Methods Thirty Sprague-Dawley rats were randomly divided into three groups （n = 10） ： the lipopolysaccharide （LPS）-induced model group, the sTNF-αR-Fc treatment group and the normal controls. Blood pressure of the rats was monitored by multi-channels biological signal analysis system, soluble TNF-α produced by splenocytes was determined by flow cytometry and TNF-α mRNA in the liver and heart was analyced by RT-PCR. Results In LPS-induced model group, expression of TNF-α mRNA increased, but blood pressure and survival rate decreased in comparison with control group （P 〈 0.05）. In sTNF-αR-Fc treatment group, expressions of TNF-α and IL-6 decreased, but survival rate increased significantly （P 〈 0.05）. Conclusion sTNF-αR-Fc can enhance the survival rate of septic shock rats by inhibiting the production of TNF-α. Therefore, it may have therapeutic value in seotic shock.
出处
《上海交通大学学报（医学版）》
CAS
CSCD
北大核心
2007年第8期909-912,共4页
Journal of Shanghai Jiao tong University:Medical Science
基金
上海市科技发展基金(034119943)~~
