论文部分内容阅读
目的:通过观察二参汤对心肌缺血大鼠血清学和组织学相关指标的影响,探讨二参汤抗心肌缺血的机制。方法:将健康Wistar大鼠用随机数字表法分为5组,二参汤高、中、低剂量组(100,50,20 g·kg-1),空白对照组和模型组,每组10只。二参汤连续ig 14 d后ip注射5 mg·kg-1异丙肾上腺素(ISO)造成心肌缺血性损伤模型后观察心电图标Ⅱ导联变化,血清血栓素A2(TXA2)、前列环素(PGI2)含量的变化及对心肌细胞凋亡相关基因Bax mRNA,Bcl-2 mRNA的表达的影响。结果:与模型组相比,二参汤组在注射ISO后5～30 min各时间段均见T波明显回落(P<0.05);二参汤组均可不同程度降低血清TXA2的含量,二参汤高剂量组(102.16±9.41)μg·L-1显著低于模型组(188.81±38.70)μg·L-1(P<0.05),增加血清PGI2的含量,二参汤高剂量组(112.10±10.45)μg·L-1显著高于模型组(36.10±4.26)μg·L-1(P<0.05),调整TXA2/PGI2的平衡;二参汤能抑制心肌组织Bax mRNA的表达,上调Bcl-2 mRNA的表达(P<0.05),保持Bcl-2 mRNA/Bax mRNA的平衡。结论:二参汤通过调节PGI2/TXA2的平衡,从而抑制血管内皮炎症性改变,保护血管内皮功能,发挥抗心肌缺血作用,通过调节Bcl-2mRNA/BAXmRNA的平衡,调整细胞凋亡基因平衡,抑制过度凋亡保护心肌细胞,达到抗心肌缺血作用。
OBJECTIVE: To observe the effect of ErShenTang on serological and histological related indexes of myocardial ischemia in rats and to explore the mechanism of ErShenTang against myocardial ischemia. Methods: The healthy Wistar rats were randomly divided into 5 groups: Erzhi Tang high, medium and low dose groups (100, 50, 20 g · kg -1), blank control group and model group, with 10 only. Erjintang Decoction for 14 days was injected ip with 5 mg · kg-1 of isoproterenol (ISO) to induce myocardial ischemic injury model. The change of ECG Ⅱ lead, serum TXA2, prostacyclin (PGI2) in cardiomyocytes and the expression of Bax mRNA and Bcl-2 mRNA in cardiomyocytes. Results: Compared with the model group, the T wave was significantly decreased in ErShen decoction group (P <0.05) at 5 ~ 30 min after injection of ISO, while the levels of TXA2 in ErSeng decoction group decreased to some extent. (102.16 ± 9.41) μg · L-1 in Shen-Tang high-dose group was significantly lower than that in model group (188.81 ± 38.70) μg · L-1 (P <0.05) ± 10.45) μg · L-1 was significantly higher than that of the model group (36.10 ± 4.26) μg · L-1 (P <0.05), and the balance of TXA2 / PGI2 was adjusted; Er Shen decoction could inhibit the expression of Bax mRNA and Bcl- -2 mRNA expression (P <0.05), maintaining Bcl-2 mRNA / Bax mRNA balance. Conclusion: Er-Shen-Tang can regulate the balance of PGI2 / TXA2, inhibit the inflammatory changes of vascular endothelium, protect the function of vascular endothelium and exert anti-myocardial ischemia. By regulating the balance of Bcl-2mRNA / BAXmRNA, Inhibit excessive apoptosis protect myocardial cells, to anti-myocardial ischemia.