Effects ofAntrodia camphorata on viability, apoptosis, [Ca2+]i, and MAPKs phosphorylation in MG63 human osteosarcoma cells

Autor: Chao-Chuan Chi, Shiuh-Inn Liu, Hsing-Hao Su, Sau-Tung Chu, Chung-Ren Jan, San-Jung Kuo, Jong-Khing Huang, Chin-Man Ho, Yih-Chau Lu, I-Shu Chen, Chun-Jen Huang, Jue-Long Wang, Chorng-Chih Huang, Shu-Shong Hsu
Rok vydání: 2007
Předmět:
Zdroj: Drug Development Research. 68:71-78
ISSN: 1098-2299
0272-4391
DOI: 10.1002/ddr.20168
Popis: The present study explored the effect of Antrodia camphorata (AC) on viability, apoptosis, mitogen-activated protein kinases (MAPKs) phosphorylation, and Ca2+ regulation in MG63 human osteosarcoma cells. AC (25–50 µg/ml) did not affect cell viability, but at 100–200 µg/ml decreased viability and induced apoptosis in a concentration-dependent manner. AC at concentrations of 25–200 µg/ml did not alter basal [Ca2+]i, but at 25 µg/ml decreased [Ca2+]i increases induced by ATP, bradykinin, histamine, and thapsigargin. ATP, bradykinin, and histamine increased cell viability while thapsigargin decreased it. AC (25 µg/ml) pretreatment failed to alter bradykinin- and thapsigargin-induced effects on viability, but potentiated ATP- and histamine-induced increases in viability. Immunoblotting showed that MG63 cells did not have background phospho-JNK and phospho-p38 mitogen-activated protein kinases (MAPKs); and AC did not induce the phosphorylation of these two MAPKs. Conversely, the cells had significant background phospho-ERK MAPK that was inhibited by 200 µg/ml AC. The ERK-specific inhibitor PD98059 also induced cell death. Collectively, in MG63 cells, AC exerted multiple effects on viability and [Ca2+]i, caused apoptosis probably via inhibition of ERK MAPK phosphorylation. Drug Dev Res 68:71–78, 2007. © 2007 Wiley-Liss, Inc.
Databáze: OpenAIRE
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