甲酰化肽样受体介导脂多糖诱导的白细胞趋化反应及虎杖甙的调节作用研究

目的：初步研究虎杖甙（PD）对脂多糖刺激下白细胞趋化活性调节的机制。 方法： 用趋化小室方法测定虎杖甙对LPS刺激下多形核白细胞（PMN）趋化活性及转染了甲酰化肽样受体（FPRL1）基因的293细胞（FPRL1/293）趋化活性的影响。 结果： LPS及LPS刺激的PMN上清可增强多形核白细胞的趋化反应；同样LPS刺激下转染了甲酰化肽样受体基因的293细胞的趋化性显著升高。而PD可下调LPS刺激引起的PMN和FPRL1/293细胞的趋化性升高。 结论： 甲酰化肽样受体FPRL1可能参与介导脂多糖引起的白细胞趋化反应，PD可能通过抑制白细胞趋化因子的分泌和下调甲酰化肽样受体活性来调节细胞的趋化性。

Role of FPRL1 in the chemotaxis of polymorphonuclear leukocytes stimulated by LPS and its regulation by polydatin

AIM: To investigate the chemotaxis mechanisms of polymerphonuclear leukocytes (PMNs) under the stimulation of LPS and its regulation by polydatin (PD). METHODS: Chemotactic chamber assay was used to investigate the regulatory role of formyl peptide receptor like-1 (FPRL1) in the chemotaxis of PMNs in response to LPS and PD. RESULTS: LPS increased the secretion of PMN chemotactic factor and up-regulated the function of formyl peptide receptor like-1. PD did not obviously affect the chemotactic factor secretion in normal PMN and the function of formyl peptide receptor like-1, but it significantly reduced the rise of chemotactic factor excretion in PMNs caused by LPS stimulation and PMNs transfected with formyl peptide receptor like-1. CONCLUSION: FPRL1 may mediate LPS-induced PMN chemotaxis, and PD regulates PMN chemotaxis by down-regulating the secretion of chemokine and the function of FPRL1 and may play a crucial role in the treatment of inflammation.