首页> 中文期刊> 《中国现代手术学杂志》 >血必净对尿源性SIRS猪肾组织细胞因子的影响

血必净对尿源性SIRS猪肾组织细胞因子的影响

             

摘要

目的 观察血必净注射液对尿源性SIRS猪肾组织细胞因子表达的影响,探讨血必净治疗尿源性SIRS的作用机制. 方法 健康实验猪45头按随机数字表法分为假手术对照组、模型组和血必净治疗组3组,每组15只,每组所有动物按时间点又分为术后0、4、6、12和24 h5个时间点亚组.建立尿源性SIRS猪模型.应用RT-PCR法检测肾组织中TNF-α、IL-6、IL-10、NF-κB p65mRNA的表达;采用Western blot法检测肾组织中NF-κB的活性. 结果 模型组猪的SIRS表现最为明显,血必净治疗组SIRS表现明显较轻.模型组猪肾组织TNF-α、IL-6、NF-κB p65mRNA的表达以及NF-κB的蛋白表达显著高于假手术组(P<0.05);血必净治疗组较模型组的TNF-α、IL-6、NF-κB p65mRNA的表达以及NF-κB的蛋白表达显著降低(P<0.01);IL-10 mRNA的表达情况则与之相反. 结论 血必净通过抑制NF-κB活性、上调IL-10、下调TNF-α,IL-6及NF-κB的表达而达到治疗尿源性SIRS的作用.%Objective To investigate the mechanism of Xuebijing injection(XBJ) in the treatment of u-rine-derived SIRS by observing its effect on the expression of TNF-a, IL-6, IL-10 and NF-kB in the renal tissue of pigs with urine-derived SIRS. Methods 45 healthy pigs in experiments were randomly divided into sham-operation group (control group) , SIRS model group, and XBJ treatment group. Each group was 15 and further divided into five observation points according to the time of operation, which were postoperative 0, 4, 6, 12 and 24h. SIRS animal model (SIRS model group) was established by injection the flush perfusion fluid with autolo-gous cecum contents into the pelvis. Application of RT-PCR was used to detect the kidney tissues of TNF-a, IL-6, IL-10 and NF-kB p65 mRNA expressions. And adoption of the Western blot was used to detect the kidney tissues of NF-kB activity. Results The clinical manifestation of urine-derived SIRS was the most evident in SIRS group. Their manifestation was improved in XBJ treatment group as compared with SIRS group. The expression of TNF-a, IL-6 and NF-kB was obviously up-regulated but IL-10 expression was down-regulated in SIRS group as compared with control group(P <0.05). The expression of TNF-a, IL-6 and NF-kB was obviously down-regulated but IL-10 expression was up-regulated in XBJ treatment group as compared with SIRS group (P <0. 01). Conclusion XBJ injection plays a role through inhibiting NF-kB activity, up-regulating IL-10 expression, and down-regulating expression of TNF-a, IL-6 and NF-kB in the urine-derived SIRS.

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