Baicalein-Induced Apoptosis via Endoplasmic Reticulum Stress Through Elevations of Reactive Oxygen Species and Mitochondria Dependent Pathway in Mouse-Rat Hybrid Retina Ganglion Cells (N18).

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Title:	Baicalein-Induced Apoptosis via Endoplasmic Reticulum Stress Through Elevations of Reactive Oxygen Species and Mitochondria Dependent Pathway in Mouse-Rat Hybrid Retina Ganglion Cells (N18).
Authors:	李玉菁(Yu-Ching Li)、林慧茹(Hui-Ju Lin)、楊仁宏(Jen-Hung Yang)、楊家欣(Yang Jai-Sing)、何恆堅(Heng-Chien Ho)、張淑貞(Shu-Jen Chang)、夏德椿(Te-Chun Hsia)、呂旭峰(Hsu-Feng Lu)、黃安正(An-Cheng Huang)、鍾景光(Jing-Gung Chung)*
Contributors:	生命科學院生物科技學系;中國附醫醫學研究部
Keywords:	Baicalein;Reactive oxygen species (ROS);Cytochrome c;Cytoplasmic Ca2+;Caspase-3;Mitochondrial death pathway;1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N-tetraacetic acid (BAPTA);Apoptosis
Date:	2009.03
Issue Date:	2009-08-25 14:39:44 (UTC+8)
Abstract:	Studies were designed to investigate the effects of baicalein on mouse–rat hybrid retina ganglion cells (N18) to better understand its effect on apoptosis and apoptosis-related genes in vitro. Cell viability, reactive oxygen species (ROS), cytoplasmic Ca2+, mitochondrial membrane potential (MMP), apoptosis induction, and caspases-3 activity were examined by flow cytometric assay. Apoptosis-associated proteins such as p53, Bax, Bcl-2, cytochrome c, and caspase-3 were examined by Western blot. We demonstrated the increase in the levels of p53, Bax, and cytochrome c and decrease in the level of Bcl-2, which are associated with the induction of apoptotic cell death after 24 h treatment with baicalein in N18 cells. Baicalein induced an increase in the cytoplasmic levels of ROS and Ca2+ in 1 h and reached their peak at 3 h, and thereafter a loss of MMP by flow cytometry. We also demonstrated a release of the cytochrome c from mitochondria into cytosol and an activation of caspase-3, which led to the occurrence of apoptosis in N18 cells treated with baicalein by Western blot. Pretreatment was conducted with BAPTA (intracellular calcium chelator) in baicalein-treated cells, the decline of MMP was recovered, and the increase in the level of cytoplasmic Ca2+ was suppressed, and the proportion of apoptosis was also markedly diminished. In conclusion, our data suggests that oxidative stress and cellular Ca2+ modulates the baicalein-induced cell death via a Ca2+-dependent mitochondrial death pathway in N18 cells.
Relation:	NEUROCHEMICAL RESEARCH 34(3 )418 ~429
Appears in Collections:	[Department of Biological Science and Technology] Journal articles

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