Song Ho Sun, Ko Myung Soo, Jo Young Soo, Whang Wan Kyunn, Sim Sang Soo
College of Pharmacy, Chung-Ang University, 221 Huksuk-dong, Dongjak-Gu, Seoul, 156-756, Korea.
Arch Pharm Res. 2015 Oct;38(10):1913-20. doi: 10.1007/s12272-015-0601-z. Epub 2015 Apr 22.
To investigate the inhibitory effect of acteoside on the process of exocytosis induced by melittin, we measured Ca(2+) mobilization, arachidonic acid (AA) release and catecholamine exocytosis in PC12 chromaffin cells. Melittin significantly increased the intracellular Ca(2+) mobilization via receptor-operated calcium channel but not the intracellular Ca(2+) release. It caused AA release via activation of Ca(2+)-dependent phospholipase A2 (PLA2) and catecholamine secretion in a dose-dependent manner. Acteoside dose-dependently inhibited the release of AA and intracellular Ca(2+) mobilization induced by melittin. Acteoside reduced the catecholamine release and raised the amount of intracellular chromogranin A which is co-released with catecholamine from melittin-stimulated PC12 cells. Taken together, our results suggest that acteoside could suppress the exocytosis via inhibition of Ca(2+)-dependent PLA2 and extracellular Ca(2+) influx in PC12 cells stimulated by melittin.
为了研究毛蕊花糖苷对蜂毒素诱导的胞吐作用过程的抑制作用，我们检测了PC12嗜铬细胞中的Ca(2+)动员、花生四烯酸（AA）释放和儿茶酚胺胞吐作用。蜂毒素通过受体操纵的钙通道显著增加细胞内Ca(2+)动员，但不增加细胞内Ca(2+)释放。它通过激活Ca(2+)依赖性磷脂酶A2（PLA2）引起AA释放，并以剂量依赖的方式导致儿茶酚胺分泌。毛蕊花糖苷剂量依赖性地抑制蜂毒素诱导的AA释放和细胞内Ca(2+)动员。毛蕊花糖苷减少了儿茶酚胺释放，并增加了细胞内嗜铬粒蛋白A的量，嗜铬粒蛋白A与蜂毒素刺激的PC12细胞中的儿茶酚胺共同释放。综上所述，我们的结果表明，毛蕊花糖苷可以通过抑制Ca(2+)依赖性PLA2和细胞外Ca(2+)内流来抑制蜂毒素刺激的PC12细胞中的胞吐作用。
