论文部分内容阅读
用体外培养的牛肺动脉内皮细胞单层(EC)研究过氧化氢(H_2O_2)对内皮细胞-中性粒细胞(EC-PMN)粘附的影响及其机理。不同浓度H_2O_2(10~(-3),10~(-2),10~(-1) mol/L)促进EC侬赖性的PMN粘附,10~(-2)mol/L作用最强,使PMN粘附率增加1.3倍。血小板激活因子(PAF)受体拮抗剂SRI 63-441预处理PMN对H_2O_2引起的EC-PMN粘附没有影响,预处理EC可显著降低粘附率。磷脂酶A_2抑制剂对溴苯酰基溴、钙调蛋白抑制剂氯丙嗪和钙离子螯合剂EGTA预处理EC都能显著降低H_2O_2引起的EC-PMN粘附。结果提示H_2O_2激活EC,细胞外Ca~(2+)内流,同时可能有细胞贮存Ca~(2+)释放,并与鲺调蛋白结合,激活磷脂酶A_2,起动PAF合成代谢,促进EC-PMN粘附。
The effect and mechanism of hydrogen peroxide (H 2 O 2) on the adhesion of endothelial cells to neutrophils (EC-PMN) were studied by using bovine pulmonary artery endothelial monolayer (EC) cultured in vitro. Different concentrations of H 2 O 2 (10 -3, 10 -2, 10 -1 mol / L) promoted the PMN adhesion of EC-Nong Lai, and the effect of 10 -2 mol / L was the strongest , So PMN adhesion rate increased 1.3 times. Platelet-activating factor (PAF) receptor antagonist SRI 63-441 pretreatment PMN had no effect on H 2 O 2 -induced EC-PMN adhesion. Pretreatment of EC could significantly reduce the adhesion rate. Phospholipase A2 inhibitor bromophenacylbromide, calmodulin inhibitor chlorpromazine and calcium ion chelator EGTA pretreatment EC can significantly reduce the H_2O_2 induced EC-PMN adhesion. The results suggest that H 2 O 2 activates EC and extracellular Ca 2+ influx, and may release Ca 2+ from the cells and binds to the hypoglycemic protein to activate phospholipase A 2 to activate the synthesis of PAF and promote EC- PMN adhesion.