Background: The aim of this study was to explore the inhibitory effect of baicalin on myocardial apoptosis induced by Ischemia-Reperfusion (I/R).

Methods: Sprague Dawley rats' heart and myocardial cells I/R model were established in vivo and vitro, then 100 mg/kg and 10 μmol/l baicalin were administrated, respectively. The experiment was randomly divided into 4 groups (n=10): Control; I/R; IR+DMEM; and I/R+baicalin groups. Postoperation, the Left Ventricular (LV) End-Diastolic Pressure (LVEDP), the maximum velocity of LV contraction (dP/dtmax) and the maximum velocity of LV diastole (dP/dtmin) were recorded by the transthoracic echocardiography; the myocardial apoptosis percentage was analyzed by Annexin VFITC/ PI and TUNEL staining, and the apoptosis gene and protein were detected by RT-PCR and western blot. Furthermore, the protein expression of the calcium-sensing receptor (CaSR) and ERK1/2 phosphorylation were observed by western blot and Fura-2-acetoxymethyl ester. Moreover, primary rats’ cardiomyocytes were cultured and ERK1/2 specific inhibitor PD98059 was added to the culture medium. The cell survival rate, vitality and apoptosis were detected by MTT, lactate dehydrogenase (LDH) and TUNEL staining assay Kit, respectively.

Results: Our present study showed that baicalin significantly improved LV hemodynamic parameters and myocardial apoptosis in myocardial I/R injury rats. Furthermore, we found that baicalin could down-regulate the protein expression of CaSR, but up-regulate the protein expression of ERK1/2. Furthermore, when the cells were pretreated with ERK1/2 inhibitor PD98059, the cells survival rate significantly decreased, but LDH activity and apoptosis significantly increased. The results indicated that the effect of baicalin on myocardial I/R injury could be inhibited by ERK1/2 inhibitor.

Conclusion: In conclusion, our data suggests that baicalin attenuates I/R-induced myocardial injury maybe through the suppression of the CaSR/ERK1/2 signaling pathway.

背景：本研究的目的是探讨黄ical苷对缺血再灌注（I / R）诱导的心肌细胞凋亡的抑制作用。

方法：体内和体外建立Sprague Dawley大鼠的心脏和心肌细胞I / R模型，分别给药100 mg / kg和10μmol/ l黄ba苷。实验随机分为4组（n = 10）：I / R；IR + DMEM；和I / R +黄ical苷组。经胸超声心动图记录左室舒张末压（LVEDP），左室舒张压最大值（dP / dtmax）和左室舒张压最大值（dP / dtmin）。膜联蛋白VFITC / PI和TUNEL法检测心肌细胞凋亡百分率，RT-PCR和Western blot检测细胞凋亡基因和蛋白。此外，通过蛋白质印迹和Fura-2-乙酰氧基甲基酯观察到钙敏感受体（CaSR）的蛋白表达和ERK1 / 2磷酸化。此外，培养原代大鼠的心肌细胞，并将ERK1 / 2特异性抑制剂PD98059加入培养基中。用MTT，乳酸脱氢酶（LDH）和TUNEL染色检测试剂盒分别检测细胞的存活率，活力和凋亡。

结果：我们的研究表明，黄ical苷可显着改善心肌I / R损伤大鼠的左室血流动力学参数和心肌细胞凋亡。此外，我们发现黄ical苷可以下调CaSR的蛋白表达，但上调ERK1 / 2的蛋白表达。此外，当用ERK1 / 2抑制剂PD98059预处理细胞时，细胞存活率显着降低，但是LDH活性和凋亡显着增加。结果表明，ERK1 / 2抑制剂可抑制黄ical苷对心肌I / R损伤的作用。

结论：总之，我们的数据表明黄ical苷可能通过抑制CaSR / ERK1 / 2信号通路来减轻I / R引起的心肌损伤。