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.
