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作 者:胡北[1] 王常丽[1] 吴琼[1] 刘小虎[2] 贾辉[1] 马宏达[1]
机构地区:[1]沈阳军区总医院药剂科,辽宁沈阳110016 [2]辽宁省中医药研究院药理学教研室,辽宁沈阳110034
出 处:《解放军药学学报》2017年第2期116-119,共4页Pharmaceutical Journal of Chinese People's Liberation Army
基 金:2010军队中医药科研专项重点课题;No.10ZYZ101
摘 要:目的研究参芪养心滴丸对三氯甲烷、氯化钡、乌头碱诱发心律失常模型及人脐静脉内皮细胞氧化应激模型的影响。方法分别采用三氯甲烷诱发小鼠心律失常实验模型,氯化钡、乌头碱诱发大鼠心律失常实验模型,观察参芪养心滴丸对心律失常的作用。进一步考察了参芪养心滴丸对人脐静脉内皮细胞氧化应激模型的作用。结果三氯甲烷诱发小鼠心律失常实验中,参芪养心滴丸可明显降低小鼠室颤阳性率(P<0.05);参芪养心滴丸能明显推迟氯化钡诱发的大鼠心律失常模型中室性心律失常发生时间、明显减少室性心律失常持续时间和心率变化率(P<0.05);参芪养心滴丸有延长乌头碱诱发的大鼠心律失常模型的室性早搏发生时间、减少室性早搏和室性心动过速持续时间及心率变化率的作用(P<0.05);MTT法及AV-PI双染流式细胞术结果均证明参芪养心滴丸可一定程度上逆转H2O2引起的细胞凋亡,且呈一定的剂量依赖性。结论参芪养心滴丸可对抗三氯甲烷、氯化钡及乌头碱诱发的实验性心律失常作用,同时具有保护氧化应激造成的血管内皮损伤的作用。Objective To study the anti-arrythmic effect of Shenqiyangxindropping pills on arrhythmia induced by chloroform,barium chloride,aconitine and the influence on the human umbilical vein endothelial cell(HUVEC)oxidative stres model.Methods The effect of Shenqiyangxindropping pills on arrhythmia induced by chloroform in mice was observed.The arrhythmia-inducing property of barium chloride and aconitine in rats was studied in the arrhythmia animal model.Then,the effect of Shenqiyangxindropping pills on the HUVEC oxidative stress model was investigated.Results Shenqiyangxindropping pills significantly decreased the incidence of chloroform-induced ventricular fibrillation in mice(P〈0.05),delayed the onset time of ventricular arrhythmia,reduced significantly the duration of ventricular arrhythmia and the change in heart rate in rats induced by barium chloride(P〈0.05),prolonged the onset time of premature ventricualr contraction,and shortened the duration of premature ventricualr contraction and ventricular tachycardia.The results obtained in MTT and AV/PI assay showed that HUVEC apoptosis induced by H2O2 was reversed when treated with Shenqiyangxindropping pills,and that the protective effect occurred in a dose-dependent manner.Conclusion Shenqiyangxindropping pills can antagonize the experimental arrhythmia induced by chloroform,barium chloride and aconitine,thus preventing HUVEC from damage by oxidative stress reaction.
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