论文部分内容阅读
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 3高表达亦可能促进炎症的放大而不是起保护作用
Objective To investigate the effects of oleic acid plus lipopolysaccharide (LPS) on the lung tissue of rats with sequential injuried proinflammatory cytokines TNFα, IL 1 β, IL 6 and anti-inflammatory cytokines IL 4, IL 1 0, IL 1 3 mRNA expression of phase, to explore these cytokines in the systemic inflammatory response and the possible role of acute lung injury. Methods A second dose of LPS was administered to rats at 1, 4, 1, 2 and 24 hours after the first injury of oleic acid, respectively. Two sequential injured rats were detected by reverse transcription polymerase chain reaction (RT PCR) Lung tissue TNFα, IL 1 β, IL 6 and IL 4, IL 1 0, IL 1 3 mRNA expression. Results The peak of mRNA expression of TNFα and ILβ was peaked at 1h, and the peak of IL-6, IL-10 and IL-13 mRNA expression in oleic acid 4h after injury, the second injury group; oleic acid endotoxin twice sequential injury induced by proinflammatory cytokines and anti-inflammatory cytokines mRNA expression compared with mono-oleic acid injury were significantly increased (P <0 0 5). Conclusions In acute lung injury, TNF α and IL 1 β are early proinflammatory cytokines, while IL 6 plays a role in the further development of inflammation. Anti-inflammatory cytokines IL 4, IL 10 and IL 13 are also highly expressed May promote the amplification of inflammation rather than a protective effect