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目的 了解NO信号传递系统对呼吸道纤毛运动的作用机制。方法 用NO前体L 精氨酸 (L Arg)作用于培养大鼠呼吸道纤毛上皮 ,并分别将纤毛组织预孵于一氧化氮合酶 (NOS)抑制剂L NMMA ,可溶性鸟苷酸环化酶 (sGC)拮抗剂ODQ及选择性cGMP依赖的蛋白酶 (PKG)拮抗剂Rp 8 Br cGMPS后 ,再施以L Arg。以相差显微镜及成像分析技术测定纤毛运动频率 (CBF)。结果 L Arg可使CBF加快 ,其作用可被L NMMA、ODQ及Rp 8 Br cGMPS所阻断。结论L Arg可能是通过NO sGC cGMP PKG途径而使大鼠呼吸道纤毛运动加快。
Objective To understand the mechanism of NO signal transmission system on respiratory cilia movement. Methods NO precursor, L Arg, was used to induce airway ciliary epithelium in rats. The ciliated tissues were preincubated with L NMMA, a inhibitor of nitric oxide synthase (NOS), soluble guanylate cyclase (sGC) antagonist ODQ and a selective cGMP-dependent protease (PKG) antagonist Rp 8 Br cGMPS. Ciliary movement frequency (CBF) was measured by phase-contrast microscopy and imaging analysis. Results L Arg accelerated CBF and its effect was blocked by L NMMA, ODQ and Rp 8 Br cGMPS. Conclusions L Arg may accelerate the airway cilia in rats through the NO sGC cGMP PKG pathway.