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目的研究川芎嗪(Tetraethylpyrazine,TMP)对前列腺素F2α(PGF2α)所致心肌肥大的影响。方法利用培养的新生大鼠心肌细胞,以细胞直径大小、蛋白质含量为心肌肥大反应指标,观察药物的抗心肌肥大效应;用Fura2/AM负载的培养心肌细胞检测细胞内游离钙浓度([Ca2+]i)。结果PGF2α107mol/L使心肌细胞明显增大,蛋白质含量明显增加,并使[Ca2+]i显著升高。与PGF2α组比较,TMP106、105和104mol/L可分别使心肌细胞直径缩小36%、44%和55%(P<0.05);蛋白质含量分别减少13%、21%和24%(P<0.01);[Ca2+]i分别降低17%、37%和48%(P<0.05)。结论TMP可抑制PGF2α诱导的心肌细胞肥大,该作用可能与其抑制心肌细胞[Ca2+]i的升高有关。
Objective To study the effect of tetramethylpyrazine (TMP) on cardiac hypertrophy induced by prostaglandin F2α (PGF2α). Methods The cultured neonatal rat cardiomyocytes were used to observe the anti-cardiac hypertrophy effect by measuring cell diameter and protein content as indicators of myocardial hypertrophy. The intracellular free calcium concentration was detected by Fura2/AM-loaded cultured cardiomyocytes ([Ca2+]. i). Results PGF2α107mol/L significantly increased myocardial cells, protein content, and increased [Ca2+]i. Compared with the PGF2α group, TMP106, 105, and 104 mol/L reduced myocardial cell diameter by 36%, 44%, and 55%, respectively (P<0.05); protein content decreased by 13%, 21%, and 24%, respectively (P<0.01). [Ca2+]i decreased by 17%, 37% and 48%, respectively (P<0.05). Conclusion TMP can inhibit PGF2α-induced cardiomyocyte hypertrophy, which may be related to its inhibition of the increase of [Ca2+]i in cardiomyocytes.