Liguzinediol对普罗帕酮诱导的急性心衰大鼠心功能的影响
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国家自然科学基金(81500310,81573304);江苏省中药资源产业化过程协调创新中心(ZDXM?2?1);江苏高校“青蓝工程”资助


Effect of liguzinediol on heart function in acute heart failure rats induced by propafenone
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    摘要:

    目的:观察川芎嗪衍生物(Liguzinediol)对普罗帕酮诱导的急性心力衰竭大鼠心脏的保护作用及机制。方法:静脉注射普罗帕酮复制大鼠急性心力衰竭模型,给予不同剂量的Liguzinediol(5.0、10.0、20.0 mg/kg)及阳性药西地兰(Digilanid C 0.045 mg/kg),用RM6240多道生理信号采集处理系统记录给药0、5、10、20、40、60、90、120 min时左心室内压最大上升/下降速率(±dp/dtmax)、左心室收缩压(left ventricular systolic pressure,LVSP)、平均收缩压(mean systolic pressure,MSP)、平均舒张压(mean diastolic pressure,MDP)和心率(heart rate,HR)的变化;Western blot、q-PCR检测钙离子(Ca2+)转运相关蛋白表达并探索其作用机制。结果:Liguzinediol 5.0、10.0和20.0 mg/kg均能有效升高模型大鼠+dp/dtmax、-dp/dtmax、LVSP、MSP、MDP和HR。Western blot和q-PCR结果显示Liguzinediol可增加钙调素依赖蛋白激酶Ⅱ(Ca2+/calmodulin-dependent protein kinaseⅡ,CAMKⅡ)及其磷酸化蛋白P- CAMKⅡ、肌浆网Ca2+-ATP酶(sarcoplasmic reticulum Ca2+-ATPase2a,SERCA2a)和磷酸化受磷蛋白(P-phospholamban,P-PLN)的表达,而兰尼碱受体2(ryanodine receptor 2,RyR2)和FK506结合蛋白12.6(FK506 binding protein 12.6,FKBP12.6)表达无显著差异。结论:Liguzinediol可明显改善急性心衰大鼠的血流动力学指标,其作用机制可能是通过调控CAMKⅡ改变细胞内Ca2+浓度来增强心肌收缩力,改善心衰。

    Abstract:

    Objective:To observe the protective effect and mechanism of liguzinediol on heart function in acute heart failure rats induced by propafenone. Methods:The rat model of acute heart failure was replicated by propafenone intravenous injection,and different doses of liguzinediol(5.0,10.0 and 20.0 mg/kg)and the positive drug of digilanid C(0.045 mg/kg)were given. The left ventricular pressure was recorded by the RM6240 multichannel physiological signal acquisition and processing system for 0,5,10,20,40,60,90 and 120 min. The changes of maximum ascending/ descending rate(±dp/dtmax),left ventricular systolic pressure(LVSP),mean systolic pressure(MSP),mean diastolic pressure(MDP)and heart rate(HR)were observed,and calcium transport related protein expression was used to detect the mechanism of liguzinediol by Western blot. Results:Liguzinediol 5.0,10.0 and 20.0 mg/kg could effectively increase the +dp/dtmax,-dp/dtmax,LVSP,MSP,MDP and HR in model rats. Western blot and q-PCR results showed that the expression of Ca2+/calmodulin-dependent protein kinaseⅡ(CAMKⅡ),P-CAMKⅡ,sarcoplasmic reticulum Ca2+-ATPase2a(SERCA2a)and P-phospholamban(P-PLN)increased significantly after intervention with liguzinediol. There was no significant difference in ryanodine receptor 2(RyR2) and FK506 binding protein 12.6(FKBP12.6) expression. Conclusion:Liguzinediol can increase the intracellular calcium concentration and improve heart failure,and the mechanism may be through the regulation of CAMKⅡ.

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李文文,徐 斌,童 静,吴敬珍,景 怡,孔雪云,吴 祥,陈 琦,蔡丹凤,王素云,成 鹏,余夕潮,郭 瑞,赵凤鸣,李 伟,李 育,卞慧敏. Liguzinediol对普罗帕酮诱导的急性心衰大鼠心功能的影响[J].南京医科大学学报(自然科学版),2018,(11):1506-1511,1524

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  • 收稿日期:2018-04-28
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  • 在线发布日期: 2018-12-03
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