映山红花总黄酮对大鼠心肌细胞收缩性的影响及其机制
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摘要
目的探讨映山红花总黄酮(TFR)对大鼠心肌细胞收缩性的影响及其可能机制。方法利用图像分析系统观察原代培养新生大鼠心肌细胞收缩幅度及收缩频率的变化,并用钙离子成像系统测定细胞内游离的Ca2+含量。结果10、100 nmol/L人尾加压素Ⅱ(h UⅡ)显著加快心肌细胞收缩频率,10 nmol/L h UⅡ可增强心肌细胞收缩幅度,但100nmol/L h UⅡ却降低心肌细胞收缩幅度; TFR 300 mg/L可显著地减慢大鼠心肌细胞收缩频率和增强心肌细胞的收缩幅度,TFR在33. 3～300 mg/L范围内,可明显地抑制100nmol/L h UⅡ诱导的心肌细胞收缩频率的增快、收缩幅度的降低及细胞内游离的Ca2+含量的增加。结论 TFR可减慢大鼠心肌细胞收缩频率,增强其收缩性,其作用可能与降低心肌细胞内游离的Ca2+含量有关。
Objective To investigate the total flavones of rhododendra( TFR) on contractility of rat myocardial cells and its possible mechanism. Methods The contraction amplitude and contraction frequency of primary cultured rat myocardial cells were observed by image analysis system. The intracellular free Ca2 +content was measured by calcium ion imaging system. Results 10 and 100 nmol/L h U Ⅱ significantly accelerated the contraction frequency of myocardial cells,and 10 nmol/L hU Ⅱ increased the contraction amplitude of myocardial cells,but 100 nmol/L hU Ⅱ reduced the contraction amplitude of myocardial cells. TFR 300 mg/L significantly slowed the contraction frequency of rat myocardial cells and increased the contraction amplitude. TFR in the range of 33. 3 ～ 300 mg/L could significantly inhibit the increase of contraction frequency,the decrease of contraction amplitude and the increase of intracellular free Ca2 +content induced by 100 nmol/L h U Ⅱ. Conclusion TFR can slow down the contraction frequency of myocardial cells and increase its contractility,which may be related to the decrease of free Ca2 +content in myocardial cells.
Objective To investigate the total flavones of rhododendra( TFR) on contractility of rat myocardial cells and its possible mechanism. Methods The contraction amplitude and contraction frequency of primary cultured rat myocardial cells were observed by image analysis system. The intracellular free Ca2 +content was measured by calcium ion imaging system. Results 10 and 100 nmol/L h U Ⅱ significantly accelerated the contraction frequency of myocardial cells,and 10 nmol/L hU Ⅱ increased the contraction amplitude of myocardial cells,but 100 nmol/L hU Ⅱ reduced the contraction amplitude of myocardial cells. TFR 300 mg/L significantly slowed the contraction frequency of rat myocardial cells and increased the contraction amplitude. TFR in the range of 33. 3 ～ 300 mg/L could significantly inhibit the increase of contraction frequency,the decrease of contraction amplitude and the increase of intracellular free Ca2 +content induced by 100 nmol/L h U Ⅱ. Conclusion TFR can slow down the contraction frequency of myocardial cells and increase its contractility,which may be related to the decrease of free Ca2 +content in myocardial cells.
引文
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[2] Satiroglu O,Uydu H A,Durakoglugil M E,et al. The relationships of isolated coronary artery ectasia with Urotensin 2 levels,hypertension and other atherosclerotic risk factors[J]. Acta Medica Mediterr,2015,31(1):149-53.
[3] Han J,He G W,Chen Z W. Protective effect and mechanism of total flavones from rhododendron simsii planch on endothelium-dependent dilatation and hyperpolarization in cerebral ischemiareperfusion and correlation to hydrogen sulphide release in rats[J]. Evid Based Complement Alternat Med, 2014,2014:904019.
[4] Jiao Y,Fan Y F,Wang Y L,et al. Protective effect and mechanism of total flavones from rhododendron simsii planch flower on cultured rat cardiomyocytes with anoxia and reoxygenation[J].Evid Based Complement Altrenat Med,2015,2015:863531.
[5] Cheng X,Zhang J,Chen Z. Effects of total flavone from rhododendron simsii planch flower on postischemic cardiac dysfunction and cardiac remodeling in rats[J]. Evid Based Complement Altrenat Med,2017,2017:5389272.
[6] Luo S Y,Chen S,Qin Y D,et al. Urotensin-Ⅱreceptor antagonist SB-710411 protects rat heart against ischemia-reperfusion injury via RhoA/ROCK pathway[J]. PLo S One,2016,11(1):e0146094.
[7] Gao S,Oh Y B,Park B M,et al. UrotensinⅡprotects ischemic reperfusion injury of hearts through ROS and antioxidant pathway[J]. Peptides,2012,36(2):199-205.
[8] Dong X,Ye X,Song N,et al. Urotensin II promotes the production of LTC4 in rat aortic adventitial fibroblasts through NF-κB-5-LO pathway by p38 MAPK and ERK activations[J]. Heart Vessels,2013,28(4):514-23.
[9] Adebiyi A. RGS2 regulates urotensin II-induced intracellular Ca2+elevation and contraction in glomerular mesangial cells[J].J Cell Physiol,2014,229(4):502-11.
[10] Al K H,Hafiane A,You Z,et al. Circulating levels of the vasoactive peptide urotensin II in patients with acute coronary syndrome and stable coronary artery disease[J]. Peptides,2014,55(5):151-7.
[11] Shimizu I. Physiological and pathological cardiac hypertrophy[J].J Mol Cell Cardiol,2016,97:245-62.
[12] Ibrahim M,Nader A,Yacoub M H,et al. Manipulation of sarcoplasmic reticulum Ca2+release in heart failure through mechanical intervention[J]. J Physiol,2015,593(15):3253-9.
[13] Luo S Y,Xu Q H,Peng G,et al. The protective effect of total flavones from rhododendron simsii planch on myocardial ischemia/reperfusion injury and its underlying mechanism[J]. Evid-Based Compl Alt,2018,2018:6139372.