Amlodipine-induced toxicity has detrimental effects on cardiac cells. The aim of this study was to examine the effect of lipid emulsion on decreased H9c2 rat cardiomyoblast viability induced by amlodipine toxicity. The effects of amlodipine, lipid emulsion, LY 294002, and glibenclamide, either alone or in combination, on cell viability and count, apoptosis, and expression of cleaved caspase-3 and -8, and Bax were examined. LY 294002 and glibenclamide partially reversed lipid emulsion-mediated attenuation of decreased cell viability and count induced by amlodipine. Amlodipine increased caspase-3 and -8 expression, but it did not alter Bax expression. LY 294002 and glibenclamide reversed lipid emulsion-mediated inhibition of cleaved caspase-3 and -8 expression induced by amlodipine. Lipid emulsion inhibited early and late apoptosis induced by amlodipine. LY 294002 and glibenclamide inhibited lipid emulsion-mediated inhibition of late apoptosis induced by amlodipine, but they did not significantly alter lipid emulsion-mediated inhibition of early apoptosis induced by amlodipine. Lipid emulsion decreased amlodipine-induced TUNEL-positive cells. These results suggest that lipid emulsion inhibits late apoptosis induced by amlodipine at toxic dose via the activation of phosphoinositide-3 kinase and ATP-sensitive potassium channels in the extrinsic apoptotic pathway.

氨氯地平引起的毒性对心脏细胞有不利影响。本研究的目的是检查脂质乳剂对氨氯地平毒性诱导的 H9c2 大鼠心肌细胞活力降低的影响。检查了氨氯地平、脂质乳剂、LY 294002 和格列本脲单独或联合使用对细胞活力和计数、细胞凋亡以及裂解的 caspase-3 和 -8 以及 Bax 表达的影响。LY 294002 和格列本脲部分逆转了脂质乳液介导的氨氯地平诱导的细胞活力和细胞计数降低的衰减。氨氯地平增加了 caspase-3 和 -8 的表达，但没有改变 Bax 的表达。LY 294002 和格列本脲逆转脂质乳液介导的氨氯地平诱导的裂解 caspase-3 和 -8 表达抑制。脂质乳液抑制氨氯地平诱导的早期和晚期细胞凋亡。LY 294002 和格列本脲抑制脂质乳液介导的氨氯地平诱导的晚期细胞凋亡，但它们没有显着改变脂质乳液介导的氨氯地平诱导的早期细胞凋亡。脂质乳液减少了氨氯地平诱导的 TUNEL 阳性细胞。这些结果表明，脂质乳剂通过激活外源性凋亡途径中的磷酸肌醇 3 激酶和 ATP 敏感钾通道来抑制毒性剂量的氨氯地平诱导的晚期细胞凋亡。脂质乳液减少了氨氯地平诱导的 TUNEL 阳性细胞。这些结果表明，脂质乳剂通过激活外源性凋亡途径中的磷酸肌醇 3 激酶和 ATP 敏感钾通道来抑制毒性剂量的氨氯地平诱导的晚期细胞凋亡。脂质乳液减少了氨氯地平诱导的 TUNEL 阳性细胞。这些结果表明，脂质乳剂通过激活外源性凋亡途径中的磷酸肌醇 3 激酶和 ATP 敏感钾通道来抑制毒性剂量的氨氯地平诱导的晚期细胞凋亡。