科研之友
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摘要
Resveratrol is a natural compound that affects cellular Ca2 homeostasis and viability in different cells. This study examined the effect of resveratrol on cytosolic free Ca2 concentrations ([Ca2 ](i)) and viability in PC3 human prostate cancer cells. The Ca2 -sensitive fluorescent dye fura-2 was used to measure [Ca2 ](i) and WST-1 was used to measure viability. Resveratrol-evoked [Ca2 ](i) rises concentration-dependently. The response was reduced by removing extracellular Ca2 . Resveratrol-evoked Ca2 entry was not inhibited by nifedipine, econazole, SKF96365 and the protein kinase C inhibitor GF109203X, but was nearly abolished by the protein kinase C activator phorbol 12-myristate 13 acetate. In Ca2 -free medium, treatment with the endoplasmic reticulum Ca2 pump inhibitor 2,5-di-tert-butylhydroquinone decreased resveratrol-evoked rise in [Ca2 ](i). Conversely, treatment with resveratrol inhibited BHQ-evoked rise in [Ca2 ](i). Inhibition of phospholipase C with U73122 did not alter resveratrol-evoked rise in [Ca2 ](i). Previous studies showed that resveratrol between 10 and 100 mu M induced cell death in various cancer cell types including PC3 cells. However, in this study, resveratrol (1-10 mu M) increased cell viability, which was abolished by chelating cytosolic Ca2 with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetra-acetic acid-acetoxymethyl ester (BAPTA/AM). Therefore, it is suggested that in PC3 cells, resveratrol had a dual effect on viability: at low concentrations (1-10 mu M) it induced proliferation, whereas at higher concentrations it caused cell death. Collectively, our data suggest that in PC3 cells, resveratrol-induced rise in [Ca2 ](i) by evoking phospholipase C-independent Ca2 release from the endoplasmic reticulum and Ca2 entry, via protein kinase C-regulated mechanisms. Resveratrol at 1-10 mu M also caused Ca2 dependent cell proliferation.
- 出版日期2013-10
- 单位中山大学; 长春大学
