地塞米松对LPS诱导的小鼠24p3 mRNA表达的影响

Effects of dexamethasone on lipopolysaccharide-induced mouse 24p3 mRNA expression

采用逆转录聚合酶链式反应(RT-PCR)方法研究了脂多糖(lipopolysaccharide,LPS)诱导的炎症中小鼠免疫器官脾脏和胸腺中24p3 mRNA含量的变化以及糖皮质激素地塞米松(DEX)对它的影响。结果表明,应急时相反应蛋白24p3不仅能被促炎症因素LPS还能被抑炎症因子DEX诱导,并且两者都呈时间依赖性的诱导24p3 mRNA的表达,但两者作用机制以及反应时间不同,DEX的作用较LPS缓慢。LPS和DEX共同作用时DEX起了主导作用,即24p3 mRNA的表达与地塞米松单独作用时趋势一致。DEX可能通过下调促炎症因子的表达来抑制由LPS诱导的应急时相反应蛋白24p3在炎症前期的高表达。24p3 mRNA的表达在胸腺和脾脏中无显著差异。

It was investigated that the expression of 24p3 mRNA in thymus and spleen of mouse treated with lipopolysaccharide and the effects of glucocorticoid dexamethasone on its expression using RT- PCR. It suggested that both pro-inflammatory factor LPS and anti-inflammatory cytokine dexamethasone could induce the expression of the acute phase protein 24p3 in the manner of time-dependent, but the mechanism and time of reaction of the two factors were different. Dexamethasone had a slowly effect on mouse compared to LPS. The expression of 24p3 in mouse treated with dexamethasone and LPS was similar to that in mouse treated with dexamethasone lonely. It suggested that dexamethasone may play the primary role in this process. Dexamethasone may inhibit LPS-induced 24p3 expression in the early stage by down-regulating the expression of pro-inflammatory cytokines. There was no significant deviation of the expression of 24p3 mRNA in mouse thymus and spleen.