磷脂酶A2激活介导中性粒细胞凋亡

Phospholipose A2 Activation mediate neutrophil apoptosis

  • 摘要: 目的: 探讨磷脂酶A2(PLA2)活性的变化对中性粒细胞凋亡的影响。方法: 采用光镜、电镜、DNA电泳和FACS等方法,分析了磷脂酶A2内外源性激活剂和抑制剂对大鼠中性粒细胞凋亡的影响。结果: 脂多糖(LPS1μg/ml)和钙离子载体(A231871μmol/L)等PLA2激动剂分别在共同培养6h和12h之内促进中性粒细胞凋亡,而PLA2阻断剂4-溴苯甲酰溴甲烷(p-BPB 0.01~1mmol/L)可明显减弱上述激动剂的促凋亡作用。但另一种PLA2非特异性抑制剂氯喹和血小板激活因子受体拮抗剂SR27417A则无上述相同的作用。结论: 结果表明PLA2激活可促进中性粒细胞凋亡过程,但该过程可能同PLA2的代谢产物血小板激活因子的直接作用无关。

     

    Abstract: Objective: To demonstrate the role of phospholipase A2 activity (PLA2) on the apoptosis of neutrophiles. Methods: The effect of PLA2 activity on neutrophil apoptosis was investigated by light, electron microscopy, DNA agarose electrophoresis and flow cytometry analysis. Results: The results showed that the apoptosis of neutrophiles was promoted by the treatment of 1 μg/ml LPS and 1 μm A23187, in 6 hours and 12 hours respectively. The apoptosis of neutrophil was markedly delayed by a PLA2 inhibitor, 4 bromophanacyl bromid (p BPB 0.01~1 mM). Chloroquine, another PLA2 inhibitor or SR27417A, a PAF receptor antagonist, were found without such an effect as p BPB on neutrophil apoptosis. Conclusion: Results suggested that the neutrophile apoptosis may be promoted by phospholipase A2 activation, but this process may not be related with PAF, one of the important metabolites of PLA2.

     

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