PGE_2抑制LPS诱导腹腔巨噬细胞产生MIP-1α和MIP-1β

The inhibitory effect of PGE_ 2 on LPS-induced MIP-1alpha and beta by peritoneal macrophage cells

目的:在离体情况下,研究PGE2能否抑制脂多糖(LPS)诱导腹腔巨噬细胞MIP1α和MIP1β的产生。方法:制备腹腔巨噬细胞,应用夹心酶联免疫分析法(SandwichELISA)检测MIP1α和MIP1β的浓度,并应用实时逆转录聚合酶链反应(realtimeRTPCR)法检测MIP1α和MIP1βmRNA的表达。结果:PGE2抑制腹腔巨噬细胞产生MIP1α和MIP1β,呈时间依赖性和浓度依赖性,抑制发生在mRNA和蛋白质水平,PGE2对巨噬细胞的抑制作用通过EP4和EP2介导。结论:PGE2能抑制MIP1α和MIP1β产生而调节免疫反应。

Objectives： To investigate whether PGE2 has inhibitory effects on proinflammatory chemokine MIP-1α/β production by LPS activated peritoneal macrophage cells in vitro. Methods： Primary peritoneal macrophages were prepared, cultured in the presence or absence of LPS. MIP-1α/β released in the Supernatants were measured by Sandwich ELISA and mRNA expression level was measured by real-time PCR. Results： PGE2 inhibits MIP-1α/β production by peritoneal macrophages in time and dose dependent man ners. This inhibitory effects were observed at both protein and mRNA level and was mediated through EP2 and EP4 receptors. Conclusion： PGE2 inhibits LPS-induced proinflammatory chemokine MIP -1α/β, thus, has anti-inflammatory functions.