Shexiang Tongxin dropping pill protects against isoproterenol-induced myocardial ischemia in vivo and in vitro.
Shexiang Tongxin dropping pill protects against isoproterenol-induced myocardial ischemia in vivo and in vitro.
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麝香通心滴丸对异丙肾上腺素所致心肌缺血的体内外保护作用
DOI：
10.18632/oncotarget.22440
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发表时间：
2017-12-12
期刊：
影响因子：
--
通讯作者：
Zhang M
中科院分区：
文献类型：
--
作者：
Qi J;Pan W;Tan Y;Luo J;Fan D;Yu J;Wu J;Zhang M
麝香通心滴丸（STDP）是我国常用的治疗心绞痛的中药方剂。然而，其作用机制仍不清楚。本研究探讨了 STDP 对心肌缺血损伤的作用。我们构建了大鼠心肌损伤模型（异丙肾上腺素皮下注射，i.h，85 mg/kg/天，持续2天），并在4组之间进行比较：CON（对照）、ISO（缺血性损伤模型）、MET（美托洛尔）和STDP。检测血清肌钙蛋白I（cTnI）、肌酸激酶（CK）、CK-MB、乳酸脱氢酶（LDH）、α-羟基丁酸脱氢酶（α-HBD）和天冬氨酸转氨酶含量，并选择5个STDP剂量（1、10、100、1000和10000mg/kg/天），绘制剂量反应曲线。 Western-blot 用于检测细胞外信号调节激酶 1/2 (ERK1/2)、蛋白激酶 B (AKT) 和卡调节蛋白激酶 II (CamkII) 的磷酸化。此外，在1.h内施用ERK1/2抑制剂PD98059、磷脂酰肌醇-3-激酶抑制剂LY294002和CamKII抑制剂KN-93。结果：STDP组cTnI、CK、CK-MB、α-HBD、LDH显着低于ISO组（P<0.05）。 STDP 表现出剂量依赖性效应，半数最大抑制浓度为 42 mg/kg/天。 STDP 组 ERK1/2 磷酸化增强（与 ISO 相比，P<0.05），而 AKT 和 CamkII 没有变化。此外，STDP 的保护作用被 i.h 内施用 PD98059 所抵消。总之，STDP通过ERK1/2信号通路保护ISO诱导的心肌缺血性损伤，这为支持STDP治疗缺血性心脏病的临床应用提供了机制。
Shexiang Tongxin dropping pill (STDP) is a formulae of Chinese Medicine commonly used to treating angina pectoris in China. However, its mechanism of action is still yet unclear. This study investigated the roles of STDP on myocardial ischemia injury. We constructed a rat model of myocardial injury (isoproterenol subcutaneous injection, i.h, 85 mg/kg/day for 2 days), and compared among 4 groups: CON (control), ISO (ischemic injury model), MET (metoprolol), and STDP. Serum contents of Troponin I (cTnI), creatine kinase (CK), CK-MB, lactate dehydrogenase (LDH), alpha-hydroxybutyric dehydrogenase (α-HBD), and Aspartate Aminotransferase were detected and five STDP doses (1, 10, 100, 1000 and 10000 mg/kg/day) were chosen to obtain a dose-response curve. Western-blot was used to detect phosphorylations of extracellular signal-regulated kinase 1/2 (ERK1/2), protein kinase B (AKT), and camodulin kinase II (CamkII). Furthermore, an ERK1/2 inhibitor PD98059, a phosphatidylinositol-3-kinase inhibitor, LY294002, and a CamKII inhibitor, KN-93 were administered i.h. Results: cTnI, CK, CK-MB, α-HBD, and LDH were significantly lower in STDP than ISO (P<0.05). STDP exhibited a dose-dependent effect with a half maximal inhibitory concentration of 42 mg/kg/day. Phosphorylation of ERK1/2 was enhanced in the STDP group (vs. ISO, P<0.05), while AKT and CamkII were not changed. Further, the protective effects of STDP were offset by PD98059 administration i.h. In conclusion, STDP protected against the ISO-induced myocardial ischemic injury via an ERK1/2 signaling pathway, which provided a mechanism to support clinical applications of STDP as treatment for ischemic heart disease.
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影响因子：
--
作者：
Feng Y;Cheng J;Wei B;Wang Y
通讯作者：
Wang Y
DOI：
10.3390/molecules201018597
发表时间：
2015-10-14
期刊：
Molecules (Basel, Switzerland)
影响因子：
--
作者：
Chen D;Lin S;Xu W;Huang M;Chu J;Xiao F;Lin J;Peng J
通讯作者：
Peng J
影响因子：
4.6
作者：
Ryu Y;Jin L;Kee HJ;Piao ZH;Cho JY;Kim GR;Choi SY;Lin MQ;Jeong MH
通讯作者：
Jeong MH
影响因子：
5
作者：
Thoonen, Robrecht;Ernande, Laura;Cheng, Juan;Nagasaka, Yasuko;Yao, Vincent;Miranda-Bezerra, Alexandre;Chen, Chan;Chao, Wei;Panagia, Marcello;Sosnovik, David E.;Puppala, Dheeraj;Armoundas, Antonis A.;Hindle, Allyson;Bloch, Kenneth D.;Buys, Emmanuel S.;Scherrer-Crosbie, Marielle
通讯作者：
Scherrer-Crosbie, Marielle
影响因子：
4.8
作者：
Liu, JC;Baker, RE;Elsholtz, HP
通讯作者：
Elsholtz, HP