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作 者:郑萌[1] 潘瑞艳[1] 臧宝霞[1] 金鸣[1] ZHENG Meng PAN Ruiyan ZANG Baoxia JIN Ming(Department of Pharmacology , Beijing Anzhen Hospital, Capital Medical University, Belting Institute of Heart, Lung and Blood Vessel Dis- eases, Beijing 100029, China)
机构地区:[1]首都医科大学附属北京安贞医院-北京市心肺血管疾病研究所药理研究室,100029
出 处:《心肺血管病杂志》2017年第7期590-595,共6页Journal of Cardiovascular and Pulmonary Diseases
基 金:北京市中医药科技项目资助(JJ2016-07)
摘 要:目的:探讨羟基红花黄色素A(HSYA)抑制血小板活化因子(PAF)诱导的与支气管哮喘相关信号转导的研究。方法:体外培养A7r9细胞株,加入HSYA,以10-8mol/L PAF刺激后,采用MTS法检测细胞的增殖,流式细胞仪检测细胞内游离钙浓度,蛋白质印迹(Western blot)法检测蛋白激酶C(PKC)表达水平和NF-κB p65的核转移。结果:与PAF组相比,PAF+HSYA组在HSYA浓度>1.5μmol/L时,可抑制A7r5细胞的增殖(P<0.05);且可明显抑制PAF所致的细胞内游离Ca^(2+)浓度的升高(均P<0.001);HSYA浓度>3μmol/L时,可明显抑制PAF诱发PKC的表达升高和p65的核转移,并呈现出明显的浓度依赖性。结论:HSYA可抑制PAF诱发的A7r5细胞的信号转导。Objective:To study the inhibition of HSYA on the PAF-induced bronchial asthma associated signal pathway.Methods:A7r9 cell was cultured.HSYA and then 10-s mol/L PAF was add to this cell.The proliferation of the A7r5 was observed with MTS assay,the elevation of free calcium concentration of inner A7r5 cells was measured by flow cytometry assay,protein levels of PKC and nuclear translocation of NF-κBp65 were detected by western blotmethod.Results:Compared with PAF group,HSYA inhibited the proliferation of A7r5 cells (P 〈 0.05) when HSYA concentration was more than 1.5μmol/L,and significantly inhibited the increase of intracellular Ca2 + concentration induced by PAF (P 〈 0.001).In addition,HSYA inhibited PAF-induced PKC expression increased and p65 nuclear translocation when HSYA concentration was more than3 μmol/L.Conclusion:It is suggested that HSYA is active to inhibit PAF-induced signal transduction in A7r5 cell.
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