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目的 :动态观察内毒素血症新生大鼠血清肿瘤坏死因子 ( TNF- α)及可溶性TNF- α受体 ( s TNFR- )的变化及地塞米松对其的影响。方法 :健康 7日龄新生大鼠 1 80只随机分为三组 ,每组 60只。对照组 :腹腔注入与其他两组等量的 0 .9%氯化钠液 0 .1 ml;内毒素 ( LPS)组 :腹腔注射 LPS5 mg/kg;治疗组 :于注入内毒素后立即注入地塞米松 ( Dex)1 0 mg/kg。于 0、1、2、4、6及 2 4 h随机选取 1 0只断头取血 ,用双抗体夹心 EL ISA法测定血清TNF-α及 s TNFR- ,同时观察 2 4 h动物病死率。结果 :1与正常对照组相比 ,B组 TNF-α于 1 h达到峰值 ( P<0 .0 1 ) ,浓度为 0时的 32倍 ,于 6h恢复正常 ;STNF- 于 1 h也显著增高 ( P<0 .0 5 ) ,持续至 4h后逐渐下降 ,2 4 h恢复正常。 2 C组 TNF-α于 1 h明显增高 ( P<0 .0 1 ) ,但仅为 0时的 5倍 ,4h恢复正常 ,升高程度明显低于 B组 ( P<0 .0 1 ) ;STNFR- 变化趋势与 B组相似 ,升高程度也明显低于 B组 ( P<0 .0 5 )。 3新生大鼠 2 4 h病死率 B组为5 0 % ,C组 2 0 % ,两组间差异显著 ( P<0 .0 5 )。结论 :TNF-α及 TNFR参与了新生大鼠内毒素血症的病理生理过程 ,Dex通过抑制 TNF-α和 TNFR的产生而减少炎症反应 ,降低病死率 ,对新生大鼠的严重感染具有保护作用
Objective: To observe the changes of serum tumor necrosis factor (TNF-α) and soluble TNF-α receptor (s TNFR-) in neonatal rats with endotoxemia and the effect of dexamethasone on it. Methods: One hundred and eighty healthy 7-day-old neonatal rats were randomly divided into three groups of 60 rats. The control group: intraperitoneal injection of 0.1% sodium chloride solution of 0.9% sodium chloride equivalent to the other two groups; LPS group: intraperitoneal injection of LPS5 mg / kg; treatment group: injection of endotoxin immediately after injection Dexamethasone (Dex) 1 0 mg / kg. At 0, 1, 2, 4, 6 and 24 h, 10 decapitated blood samples were randomly selected for determination of serum TNF-α and TNFR-α by double antibody sandwich ELISA. The animal mortality rate at 24 h was also observed. Results: 1 Compared with the normal control group, the TNF-α peaked at 1 hour (P <0.01) in group B, 32-fold at 0 and returned to normal at 6 hours; STNF- also significantly increased at 1 hour (P <0.05), and continued to decrease gradually after 4 hours, returning to normal after 24 hours. The TNF-α level in group C was significantly higher than that in group B at 1 h (P <0.01), but only 5-fold at 0 and 4 h after transplantation. The level of TNF-α in group 2 was significantly lower than that in group B (P <0.01). The trend of STNFR- was similar to that of group B, and the increase was also significantly lower than that of group B (P <0.05). Neonatal rats 24 h mortality rate was 50% in group B and 20% in group C, with significant difference between the two groups (P <0.05). CONCLUSION: TNF-α and TNFR are involved in the pathophysiological process of endotoxemia in neonatal rats. Dex can reduce inflammation and reduce the mortality by inhibiting the production of TNF-α and TNFR, which has a protective effect on severe infection in neonatal rats