Song Qiongtao, Chu Xi, Zhang Xuan, Bao Yifan, Zhang Yuanyuan, Guo Hui, Liu Yang, Liu Hongying, Zhang Jianping, Zhang Ying, Chu Li
Hebei Medical University, No.361, East Zhongshan Road, Shijiazhuang 050017, Hebei, China.
The Fourth Hospital of Hebei Medical University, No.12, Jiankang Road, Shijiazhuang 050011, Hebei, China.
J Ethnopharmacol. 2016 Aug 2;189:157-64. doi: 10.1016/j.jep.2016.05.038. Epub 2016 May 20.
Salvianic acid A (SAA), which is the main water-soluble fraction in Radix Salviae Milthiorrhizae, has been widely applied for treating cardiovascular diseases in China.
To explore the effects of SAA against myocardial ischemia injury induced by isoproterenol (ISO) in rats and to clarify its underlying myocardial protective mechanisms based on l-type calcium channels and myocardial contractility.
The myocardial ischemia injured rat model was induced by administering ISO (85mg/kg) subcutaneously at evenly spaced intervals throughout the day and night for 2 consecutive days. Serum cardiac biomarkers were analyzed, and heart tissues were isolated and prepared for histopathology assay. The regulatory effects of SAA on the L-type calcium current (ICa-L) in rat ventricular myocytes were observed by the patch clamp technique. The IonOptix Myocam detection system was used to observe the contractility of isolated rat ventricular myocytes.
SAA significantly ameliorated changes in heart morphology and electrocardiographic patterns and reduced serum levels of creatine kinase and lactate dehydrogenase in the ISO-induced myocardial ischemia injured rat model. Meanwhile, SAA reduced ICa-L in a concentration-time dependent way with an IC50 of 1.47×10(-5)M, upshifted the current-voltage, activation, and inactivation curves of ICa-L, and significantly inhibited the amplitude of the cell shortening.
These results indicate that SAA exhibits significant cardioprotective effects against the ISO-induced myocardial ischemia injury, potentially through inhibiting ICa-L and decreasing myocardial contractility.
丹酚酸A（SAA）是丹参的主要水溶性成分，在中国已被广泛应用于治疗心血管疾病。
探讨SAA对异丙肾上腺素（ISO）诱导的大鼠心肌缺血损伤的影响，并基于L型钙通道和心肌收缩性阐明其潜在的心肌保护机制。
通过在昼夜均匀间隔皮下注射ISO（85mg/kg）连续2天诱导大鼠心肌缺血损伤模型。分析血清心脏生物标志物，并分离心脏组织并制备用于组织病理学分析。采用膜片钳技术观察SAA对大鼠心室肌细胞L型钙电流（ICa-L）的调节作用。使用IonOptix Myocam检测系统观察分离的大鼠心室肌细胞的收缩性。
在ISO诱导的心肌缺血损伤大鼠模型中，SAA显著改善心脏形态和心电图模式的变化，并降低血清肌酸激酶和乳酸脱氢酶水平。同时，SAA以浓度-时间依赖性方式降低ICa-L，IC50为1.47×10（-5）M，使ICa-L的电流-电压、激活和失活曲线上移，并显著抑制细胞缩短幅度。
这些结果表明，SAA对ISO诱导的心肌缺血损伤具有显著的心脏保护作用，可能是通过抑制ICa-L和降低心肌收缩性实现的。
