摘要
目的：观察肠缺血—再灌流过程中肠源性ＩＮＦα和ＩＬ－６ 表达的规律并探讨介导肠源性细胞因子表达的因素。方法：采用ＲＴ—ＰＣＲ和ＲＩＡ 的方法检测了肠缺血—再灌流过程中小肠组织ＴＮＦα和ＩＬ６ｍ ＲＮＡ表达及其蛋白含量的变化，并测定组织丙二醛（ＭＤＡ）含量及肠静脉血浆ＬＰＳ浓度。结果：正常情况下小肠ＴＮＦα和ＩＬ～６ｍ ＲＮＡ仅有少量表达，肠缺血１ｈ～１．５ｈ，表达已开始增加，再灌流０．５ｈ～１ｈ，表达至峰值，与肠静脉血浆内毒素（ＬＰＳ）浓度及组织丙二醛（ＭＤＡ）含量变化趋势基本一致，但表达增加的高峰略早于血浆ＬＰＳ峰值而晚于组织ＭＤＡ含量的增加。结论：肠缺血—再灌流时，肠道是早期产生炎性细胞因子的重要器官，在诱发ＳＩＲＳ中可能起重要作用；原发的缺氧、氧自由基生成及通过受损肠壁的ＬＰＳ可能均参与介导小肠炎性介质的表达。
Objective:To investigate the expressed regularity of gut TNF α and IL 6 mRNA after gut ischemia reperfusion and the factors causing the expression of gut originated inflammatory mediators.Methods:Male Wistar rats were subjected to superior mesenteric artery occlusion followed by reperfusion.The expression of gut TNF α,IL 6 mRNA and protein levels were measured by RT-PCR and RIA,and gut MDA content and intestinal venous plasma LPS concentration were determined as well.Results:The expressed TNF α and IL 6 mRNA were less in normal small intestinal tissue but enhanced at 1～1.5h post ischemia,peaking at 0.5～1h after reperfusion.TNF α and IL 6 mRNA expression was generally paralled to the changes of LPS concentration in intestinal venous plasma and MDA contented in intestinal tissue,but the expressed peaks were earlier than that of LPS and latter than that of MDA.Conclusions:During gut ischemia reperfusion small intestine was the important organ producing inflammatory cytokines,which may play an important role in inducing SIRS;Anoxia,oxygen free radicals and LPS might be involved in stimulating inflammatory mediators expression.
出处
《河北医学》
CAS
2000年第1期1-5,共5页
Hebei Medicine
