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目的：研究过氧化氢（Ｈ２Ｏ２）对肾小球系膜细胞－中性粒细胞（ＧＭＣ－ＰＭＮ）粘附的影响及其机制。方法：用体外培养的人肾小球系膜细胞与不同浓度血小板活化因子（ＰＡＦ）或Ｈ２Ｏ２作用，并以各类拮抗剂观察其对ＧＭＣ－ＰＭＮ粘附的影响。结果：不同浓度Ｈ２Ｏ２促进ＧＭＣ依赖性ＰＭＮ粘附，以１０－２ｍｏｌ／Ｌ浓度的作用最强，使ＰＭＮ粘附率增强２．２倍。用ＰＡＦ受体拮抗剂预处理ＰＭＮ对粘附无影响。预处理ＧＭＣ可显著降低粘附率，磷酯酶Ａ２抑制剂对溴基苯酰基溴、钙调蛋白抑制剂氯丙嗪和钙离子螯合剂ＥＧＴＡ预处理ＧＭＣ，均能降低Ｈ２Ｏ２引起的ＧＭＣ－ＰＭＮ粘附。结论：Ｈ２Ｏ２可促进ＧＭＣ与ＰＭＮ的粘附。Ｈ２Ｏ２的这一作用可能是通过ＰＡＦ介导的。
Objective: To investigate the effect of hydrogen peroxide (H2O2) on the adhesion of glomerular mesangial cells (PMNs) to neutrophils (GMC-PMN) and its mechanism. Methods: Human glomerular mesangial cells cultured with different concentrations of platelet activating factor (PAF) or H2O2, and various antagonists observed GMC-PMN adhesion. Results: Different concentrations of H2O2 promoted the GMC-dependent PMN adhesion, the strongest effect was at 10-2mol / L, and the PMN adhesion rate increased 2.2 times. Pretreatment of PMN with PAF receptor antagonist had no effect on adhesion. Pretreatment of GMC could significantly reduce the adhesion rate. Both phospho-esterase A2 inhibitor bromobenzyl bromide, calmodulin inhibitor chlorpromazine and calcium ion chelator EGTA pretreatment GMC could reduce the GMC-PMN induced by H2O2 Adhesion. Conclusion: H2O2 can promote the adhesion of GMC and PMN. This role of H2O2 may be mediated through PAF.