A formyl peptide contracts guinea pig lung: role of arachidonic acid metabolites.
A formyl peptide contracts guinea pig lung: role of arachidonic acid metabolites.
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甲酰基肽收缩豚鼠肺：花生四烯酸代谢物的作用。
DOI：
10.1152/jappl.1987.63.6.2450
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Drazen,JM
中科院分区：
文献类型：
--
作者：
Shore,SA;Stimler-Gerard,NP;Smith,E;Drazen,JM
我们研究了花生四烯酸代谢的环加氧酶和脂加氧酶产物在介导n -甲氧基-蛋氨酸-leucyl-苯丙氨酸（FMLP）诱导的豚鼠肺实质条收缩中的作用。环氧酶抑制剂吲哚美辛(10 (5)M)和阿司匹林(3 X 10(5)到10 (4)M),脂氧合酶抑制剂去甲二氢愈创木酸(10 (5)3 X 10(5)米),和合并后的环氧酶/脂氧合酶抑制剂1-phenyl-3-pyrazolidinone (Phenidone) (3 X 10 (5) 3 X 10 (4) M)和BW 755 c(10(5)到10 (4)M)每下降引起的最大力量引起FMLP (Fmax)和增加的浓度FMLP所需50%的Fmax (EC50)。血栓素合成抑制剂咪唑（3 × 10(-3) M）也能降低Fmax。白三烯D4受体拮抗剂FPL 55712 (5.7 × 10（-6) ~ 1.9 × 10(-5) M）增加了FMLP的EC50，而用白三烯（10(-7)M）预处理肺实质条对白三烯B4脱敏对FMLP诱导的收缩没有影响。暴露于FMLP （10(-6) M）后，豚鼠肺产生（通过高效液相色谱和放射免疫分析法测定）白三烯C4和B4，血栓素A2（通过其稳定降解产物血栓素B2测定）和前列腺素F2 α。未暴露于FMLP的肺条未显示白三烯产生的证据。我们得出结论，在豚鼠肺实质条中，响应FMLP产生的血栓素A2和白三烯C4介导了该肽诱导的很大一部分力。
We studied the role of cyclooxygenase and lipoxygenase products of arachidonic acid metabolism in mediating N-formyl-methionyl-leucyl-phenylalanine- (FMLP) induced contractions of guinea pig lung parenchymal strips. The cyclooxygenase inhibitors indomethacin (10(-5) M) and aspirin (3 X 10(-5) to 10(-4) M), the lipoxygenase inhibitor nordihydroguaiaretic acid (10(-5) to 3 X 10(-5) M), and the combined cyclooxygenase/lipoxygenase inhibitors 1-phenyl-3-pyrazolidinone (Phenidone) (3 X 10(-5) to 3 X 10(-4) M) and BW 755C (10(-5) to 10(-4) M) each caused a decrease in the maximum force induced by FMLP (Fmax) and an increase in the concentration of FMLP required to produce 50% of Fmax (EC50). The thromboxane synthesis inhibitor imidazole (3 X 10(-3) M) also decreased Fmax. The leukotriene D4 receptor antagonist FPL 55712 (5.7 X 10(-6) to 1.9 X 10(-5) M) increased the EC50 for FMLP, whereas desensitization of lung parenchymal strips to leukotriene B4 by pretreatment with this leukotriene (10(-7) M) had no effect on FMLP-induced contraction. After exposure to FMLP (10(-6) M), guinea pig lung produced (as determined by high-performance liquid chromatography and radioimmunoassay) leukotrienes C4 and B4, thromboxane A2 (as measured by its stable degradation product thromboxane B2), and prostaglandin F2 alpha. Lung strips not exposed to FMLP showed no evidence of leukotriene production. We conclude that thromboxane A2 and leukotriene C4 generated in response to FMLP mediate a substantial fraction of the force induced by this peptide in guinea pig lung parenchymal strips.