油酸-内毒素致伤大鼠肺组织TNF-α、IL-1β、IL-6和IL-4、IL-10、IL-13的mRNA表达

Studies on the expression of TNF alpha, IL-1 beta, IL-6 and IL-4, IL-10, IL-13 mRNA in lung tissue of rat with acute lung injury induced by oleic acid and lipopolysaccharide

目的 研究油酸加内毒素脂多糖 (LPS)序贯性两次致伤大鼠肺组织促炎症细胞因子TNF α、IL 1 β、IL 6和抗炎细胞因子IL 4、IL 1 0、IL 1 3的mRNA表达时相性 ,探讨这些细胞因子在全身炎症反应失控和急性肺损伤中可能的作用。方法 分别在油酸第 1次致伤后 1、4、1 2和 2 4h实施小剂量LPS第 2次致伤 ,采用逆转录多聚酶链式反应 (RT PCR)检测两次序贯性致伤大鼠肺组织TNF α、IL 1 β、IL 6和IL 4、IL 1 0、IL 1 3的mRNA表达。结果 TNF α和IL 1 β的mRNA表达高峰在油酸第 1次致伤后 1hLPS第 2次致伤组 ,而IL 6和IL 4、IL 1 0、IL 1 3的mRNA表达峰值则在油酸致伤后 4h第 2次致伤组 ;油酸 内毒素两次序贯性致伤后的促炎症细胞因子和抗炎细胞因子的mRNA表达与单油酸致伤比较均显著增强 (P <0 0 5 )。结论 在急性肺损伤中 ,TNF α和IL 1 β是早期表达的促炎细胞因子 ,而IL 6在炎症进一步发展中发挥作用 ;抗炎细胞因子IL 4、IL 1 0、IL 1

Objective To study the role of pro inflammatory cytokines tumor necrosis factorα(TNF α),interleukin 1beta(IL 1β),interleukin 6(IL 6) and anti inflammatory cytokines interleukin 4(IL 4),interleukin 10(IL 10),interleukin 13(IL 13) in acute lung injury(ALI). Methods Wistar Rats (200±50g) were randomly divided into the oleic acid(OA) and Lipoplysaccharide(LPS) induced lung injury experimental group and the only OA induced lung injury control group. The LPS(2mg/kg) was injected in rat's tail vein at the 1, 4, 12 and 24 hours after administration of OA(0.2ml/kg, iv). Reverse transcription polymerase chain reaction(RT PCR) were used to detecting the expression of TNF α, IL 1β, IL 6 and IL 4, IL 10, IL 13 mRNA in the lung tissue of rats in two groups. Results The results showed that the peak expression of TNF α and IL 1β mRNA at one hour after first hit by oleic acid, and IL 6 mRNA at four hours were observed. Others, such as IL 4, IL 10 and IL 13 mRNA, the highest levels in lung tissue at four hours after lung injury induced by oleic acid. Conclusions The results suggested that TNF α and IL 1β are presenting early phase of ALI, and that IL 6 played its important role in delayed development. The over expression of anti inflammatory cytokines IL 4, IL 10 and IL 13 may be as a promoters rather than protectors in inflammatory amplification.