【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。更多还原

【Abstract】 Objective To research if bronchial epithelium derived relaxing factor(BrEpDRF) is transducted by PI3/Akt and NO-cGMP 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 Mch 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 Mch alone statistically(P<0.01),respectively.Conclusion Under physiological condition,BrEpDRF is signalled by NO-cGMP and PI3/Akt pathway.更多还原