甘草苷对乌头碱致心肌细胞损伤的保护作用

Protective effect of Liquiritin on cardiocyte injury of neonate rat induced by aconitine

目的:观察甘草苷对乌头碱导致心肌细胞损伤的保护作用并探讨相关机制。方法:利用原代培养的乳鼠心肌细胞,观察甘草苷对乌头碱引起的心肌细胞释放乳酸脱氢酶(LDH)的影响;采用RT-PCR的方法,观察甘草苷与乌头碱配伍后对心肌细胞钙离子通道编码基因Cav1.2 mRNA以及钾离子通道编码基因Kv4.3 mRNA表达的调控作用,半定量分析甘草苷与乌头碱配伍对上述离子通道基因表达的影响。结果:甘草苷可以减低由乌头碱导致的大鼠心肌细胞LDH释放;可以拮抗由乌头碱引起的Cavl.2基因的mRNA表达升高,和Kv4.3基因的mRNA表达的降低。结论:甘草苷与乌头碱配伍可以减轻乌头碱的毒性作用,这可能与甘草苷改善了乌头碱对心肌细胞钾、钙离子通道编码基因的异常表达有关。

Objective： To explore the protective effect and mechanism of Liquiritin on cardiocyte injury of neonate rat induced by aconitine. Methods： Primary cultured neonatal rat cardiocyte was used to observe the influence of aconitine and liquiritin after incubated in the two drugs for 8 hours. The influence of the two components was examined by release of LDH （lactate dehydrogenase） of cardiocyte, and then ion channel Kv4.3 and Cavl.2 mRNA expression was examined by reverse transcriptasepolymerase chain reaction. The densities of these bands were semi-quantified. Results： Liquifitin could reduce the release of LDH from cardio-myocyte induced by aconitine （P〈0.01）. There were significant increases in abundance of Cav1.2 mRNA and significant decreases in that of Kv4.3 mRNA in aconitine group compared to those in the control group （P〈0.01）. The liquiritin could reverse the abnormal expression of Cav1.2 and Kv4.3 mRNA induced by aconitine. Conclusion： The action mechanism might be linked with that the liquiritin could suppress abnormal expression of ion channel genes Cav1.2 and Kv4.3 mRNA in neonate rat cardiomyocytes induced by aconitine.