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观察注射用重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rhu TNFR:Fc)对脂多糖(LPS)诱导的休克大鼠肠损伤的保护作用及其可能机制。SD大鼠随机分为对照组、rhu TNFR:Fc组、LPS组和rhu TNFR:Fc+LPS组,监测各组大鼠平均动脉压(MAP)计算其死亡率,检测血清中肿瘤坏死因子-α(TNF-α)含量和活性;观察小肠病理形态变化。结果表明,对照组和rhu TNFR:Fc组大鼠全部存活,MAP无变化,TNF-α含量和活性均维持较低水平;LPS组大鼠死亡率为83%,TNF-α含量和活性明显高于对照组;rhu TNFR:Fc+LPS组大鼠死亡率33%,TNF-α含量升高,其活性较LPS组明显降低,rhu TNFR:Fc还能降低LPS所致的MDA含量和MPO活性的升高并减轻LPS所致的肠病理性损伤。因此rhu TNFR:Fc对LPS诱导的休克大鼠的肠损伤有保护作用,其机制可能主要是竞争性结合TNF-α,减低TNF-α活性以及抗氧化作用。
To observe the protective effect of rhu TNFR (Fc) on human intestinal injury induced by lipopolysaccharide (LPS) and its possible mechanism. SD rats were randomly divided into control group, rhu TNFR: Fc group, LPS group and rhu TNFR: Fc + LPS group. The mean arterial pressure (MAP) of the rats in each group was calculated to calculate the mortality rate. The level of TNF- (TNF-α) content and activity; observed pathological changes of small intestine. The results showed that all the rats in the control and rhu TNFR: Fc groups survived, MAP did not change, TNF-α content and activity were maintained at a low level; the mortality rate of rats in LPS group was 83%, TNF-α content and activity were significantly higher In the control group, the rhu TNFR: Fc + LPS group had a 33% mortality rate and a higher TNF-α level than the LPS group. Rhu TNFR: Fc also reduced the MDA content and MPO activity induced by LPS Increase and reduce the intestinal pathological damage caused by LPS. Therefore, rhu TNFR: Fc has a protective effect on intestinal injury induced by LPS in rats with shock, and its mechanism may be mainly binding competitive TNF-α, reducing TNF-α activity and anti-oxidation.