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Cell Biology International (2010) 34, 109–116 (Printed in Great Britain)

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Green tea polyphenol (−)-epigallocatechin gallate suppressed the differentiation of murine osteoblastic MC3T3-E1 cells

Masayoshi Kamon, Ran Zhao and Kazuichi Sakamoto¹

Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan

Recently, various physiological effects of the tea polyphenol catechin for alleviating diseases such as cancer, arteriosclerosis, hyperlipidaemia and osteoporosis have been reported. However, the physiological effect of catechin on bone metabolism remains unclear. We examined the physiological effect of EGCG [(−)-epigallocatechin-3-gallate], which is the main component of green tea catechin, on osteoblast development using the precursor cell line of osteoblasts, MC3T3-E1, and co-culture of the osteoblasts from mouse newborn calvaria and mouse bone marrow cells. Although EGCG did not affect the viability and proliferation of MC3T3-E1 cells, EGCG inhibited the osteoblast differentiation. Furthermore, EGCG did not affect the mineralization of differentiated MC3T3-E1 cells, and reduced osteoclast formation in co-culture. These results suggest that EGCG can effectively suppress bone resorption, and can be used as an effective medicine in the treatment of the symptoms of osteoporosis.

Key words: catechin, osteoblast, polyphenol

Abbreviations: 67LR, 67 kDa laminin receptor, ALP, alkaline phosphatase, α-MEM, minimum essential medium alpha medium, BMP, bone morphogenetic protein, CSF-1, colony stimulating factor-1, EC, (−)-epicatechin, ECG, (−)-epicatechin-3-gallate, EGC, (−)-epigallocatechin, EGCG, (−)-epigallocatechin-3-gallate, FBS, fetal bovine serum, G3PDH, glyceraldehyde 3-phosphate dehydrogenase, GST, glutathione transferase, MTT, 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide, NEAA, non-essential amino acid solution, OCN, osteocalcin, RANKL, receptor activator of nuclear factor κB ligand, TRAP, tartrate-resistant acid phosphatase

¹To whom correspondence should be addressed (email sakamoto@biol.tsukuba.ac.jp).

Received 17 March 2009/23 July 2009; accepted 15 September 2009

Published as Cell Biology International Immediate Publication 15 September 2009, doi:10.1042/CBI20090011

Journal compilation © 2010 Portland Press Ltd