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新生大鼠支气管上皮衍生舒张因子信号传导

Bronchial epithelium derived relaxing factor signal transduction of neonate rat
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摘要 目的研究支气管上皮衍生舒张因子(BrEpDRF)是否经一氧化氮(NO)-3′,5′-鸟嘌呤核苷环一磷酸(cGMP)及磷脂酰三肌醇(PI3)/蛋白激酶B(Akt)通路传导。方法支气管结合的肺动脉经血栓烷A2(TXA2)类似物U46619预刺激肺动脉收缩,在PI-3激酶/Akt抑制剂LY294002和NO-GMP抑制剂ODQ存在/不存在下,测定乙酰甲胆碱(Mch)引起的血管舒张比率。结果结合支气管的肺动脉在经U46619预刺激后,Mch引起血管舒张率为39.37%;Mch中加入PI-3激酶/Akt抑制剂引起的血管舒张率为11.72%,两者比较差异有显著性,(P<0.01)。Mch中加入NO-GMP抑制剂引起的血管舒张率为2.15%,与单一Mch比较统计学上有差异,(P<0.01)。结论新生大鼠在生理条件下BrEpDRF经NO-cGMP及PI3/Akt通路传导。 Objective To research if bronchial epithelium derived relaxing factor （BrEpDRF） is transducted by PI3/Akt and NO-eGMP pathway.Methods Observe vessel relaxation rate of pulmonary artery with bronchus attached stimulated by methacholine （Mch） under/not under PI3/Akt inhibitor LY294002 or NO-GMP inhibitor ODQ after pre stimulated by U46619.Results After stimulated by U46619,the relax rate of pulmonary artery with bronchus attached is 39.37% stimulated by Mch,and the relax rate is 11.72 % stimulated by Meh with PI3/Akt inhibitor LY294002, compared significantly （ P 〈 0.01 ） ;the relax rate is 2.15 % stimulated by Mch with NO-GMP inhibitor ODQ, which is less than that of stimulated by Meh alone statistically （ P 〈 0.01） ,respectively. Conclusion Under physiological condition,BrEpDRF is signalled by NO-cGMP and PI3/Akt pathway.
作者 刘炀 刘国津 Mitchell P Fink
机构地区 吉林大学第一医院胸外科 美国匹兹堡大学重症监护医学实验室 吉林省肿瘤医院胸一科
出处 《中国实验诊断学》 北大核心 2009年第5期581-583,共3页 Chinese Journal of Laboratory Diagnosis
关键词 支气管支气管上皮衍生舒张因子 肺血管阻力 一氧化氮 一氧化氮合成酶 磷脂酰肌醇-3激酶/蛋白激 酶B途径 3' 5'-鸟嘌呤核苷环一磷酸 bronchial epithelium derived relaxing factor （ BrEpDRF ） nitric oxide （NO） nitric oxide synthase （NOS） phosphatidylinositol 3-kinase/protein kinase B（PI3/Akt ） pathway cyclic guanosine 3＇ ,5＇-monophosphate （cGMP）
分类号 R722.1 [医药卫生—儿科]
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中国实验诊断学
2009年 第5期

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