(-)-Epigallocatechin gallate induces apoptosis, via caspase activation, in osteoclasts differentiated from RAW 264.7 cells

J. H. Yun, C. S. Kim, K. S. Cho, J. K. Chai, C. K. Kim, S. H. Choi

Research output: Contribution to journalArticle

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Abstract

Background and Objective: Alveolar bone resorption is a characteristic feature of periodontal diseases and involves removal of both the mineral and the organic constituents of the bone matrix, a process mainly carried out by multinucleated osteoclast cells. (-)-Epigallocatechin gallate, the main constituent of green tea polyphenols, has been reported to induce the apoptotic cell death of osteoclasts and to modulate caspase activation in various tumor cells. In the present study, we investigated the inhibitory effect of (-)-epigallocatechin gallate on osteoclast survival and examined if (-)-epigallocatechin gallate mediates osteoclast apoptosis via caspase activation. Material and Methods: The effect of (-)-epigallocatechin gallate on osteoclast survival was examined by tartrate-resistant acid phosphatase (TRAP) staining in osteoclasts differentiated from RAW 264.7 cells. In addition, we evaluated the apoptosis of osteoclasts by (-)-epigallocatechin gallate using a DNA-fragmentation assay. Involvement of caspase in (-)-epigallocatechin gallate-mediated osteoclast apoptosis was evaluated by treatment with a general caspase inhibitor, Z-VAD-FMK. Moreover, the effect of (-)-epigallocatechin gallate on the activation of caspase-3 was assessed by a colorimetric activity assay and western blotting. Results: (-)-Epigallocatechin gallate significantly inhibited, in a dose-dependent manner, the survival of osteoclasts differentiated from RAW 264.7 cells and induced the apoptosis of osteoclasts. Treatment with (-)-epigallocatechin gallate resulted in DNA fragmentation and induced the activation of caspase-3 in RAW 264.7 cell-derived osteoclasts. Additional treatment with Z-VAD-FMK suppressed these effects of (-)-epigallocatechin gallate. Conclusion: From these findings, we could suggest that (-)-epigallocatechin gallate might prevent alveolar bone resorption by inhibiting osteoclast survival through the caspase-mediated apoptosis.

Original languageEnglish
Pages (from-to)212-218
Number of pages7
JournalJournal of Periodontal Research
Volume42
Issue number3
DOIs
Publication statusPublished - 2007 Jun 1

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Osteoclasts
Caspases
Apoptosis
Alveolar Bone Loss
DNA Fragmentation
Bone Resorption
Caspase 3
RAW 264.7 Cells
epigallocatechin gallate
Bone Matrix
Caspase Inhibitors
Polyphenols
Periodontal Diseases
Tea
Minerals
Cell Death
Western Blotting
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Periodontics

Cite this

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title = "(-)-Epigallocatechin gallate induces apoptosis, via caspase activation, in osteoclasts differentiated from RAW 264.7 cells",
abstract = "Background and Objective: Alveolar bone resorption is a characteristic feature of periodontal diseases and involves removal of both the mineral and the organic constituents of the bone matrix, a process mainly carried out by multinucleated osteoclast cells. (-)-Epigallocatechin gallate, the main constituent of green tea polyphenols, has been reported to induce the apoptotic cell death of osteoclasts and to modulate caspase activation in various tumor cells. In the present study, we investigated the inhibitory effect of (-)-epigallocatechin gallate on osteoclast survival and examined if (-)-epigallocatechin gallate mediates osteoclast apoptosis via caspase activation. Material and Methods: The effect of (-)-epigallocatechin gallate on osteoclast survival was examined by tartrate-resistant acid phosphatase (TRAP) staining in osteoclasts differentiated from RAW 264.7 cells. In addition, we evaluated the apoptosis of osteoclasts by (-)-epigallocatechin gallate using a DNA-fragmentation assay. Involvement of caspase in (-)-epigallocatechin gallate-mediated osteoclast apoptosis was evaluated by treatment with a general caspase inhibitor, Z-VAD-FMK. Moreover, the effect of (-)-epigallocatechin gallate on the activation of caspase-3 was assessed by a colorimetric activity assay and western blotting. Results: (-)-Epigallocatechin gallate significantly inhibited, in a dose-dependent manner, the survival of osteoclasts differentiated from RAW 264.7 cells and induced the apoptosis of osteoclasts. Treatment with (-)-epigallocatechin gallate resulted in DNA fragmentation and induced the activation of caspase-3 in RAW 264.7 cell-derived osteoclasts. Additional treatment with Z-VAD-FMK suppressed these effects of (-)-epigallocatechin gallate. Conclusion: From these findings, we could suggest that (-)-epigallocatechin gallate might prevent alveolar bone resorption by inhibiting osteoclast survival through the caspase-mediated apoptosis.",
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(-)-Epigallocatechin gallate induces apoptosis, via caspase activation, in osteoclasts differentiated from RAW 264.7 cells. / Yun, J. H.; Kim, C. S.; Cho, K. S.; Chai, J. K.; Kim, C. K.; Choi, S. H.

In: Journal of Periodontal Research, Vol. 42, No. 3, 01.06.2007, p. 212-218.

Research output: Contribution to journalArticle

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AU - Kim, C. S.

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AB - Background and Objective: Alveolar bone resorption is a characteristic feature of periodontal diseases and involves removal of both the mineral and the organic constituents of the bone matrix, a process mainly carried out by multinucleated osteoclast cells. (-)-Epigallocatechin gallate, the main constituent of green tea polyphenols, has been reported to induce the apoptotic cell death of osteoclasts and to modulate caspase activation in various tumor cells. In the present study, we investigated the inhibitory effect of (-)-epigallocatechin gallate on osteoclast survival and examined if (-)-epigallocatechin gallate mediates osteoclast apoptosis via caspase activation. Material and Methods: The effect of (-)-epigallocatechin gallate on osteoclast survival was examined by tartrate-resistant acid phosphatase (TRAP) staining in osteoclasts differentiated from RAW 264.7 cells. In addition, we evaluated the apoptosis of osteoclasts by (-)-epigallocatechin gallate using a DNA-fragmentation assay. Involvement of caspase in (-)-epigallocatechin gallate-mediated osteoclast apoptosis was evaluated by treatment with a general caspase inhibitor, Z-VAD-FMK. Moreover, the effect of (-)-epigallocatechin gallate on the activation of caspase-3 was assessed by a colorimetric activity assay and western blotting. Results: (-)-Epigallocatechin gallate significantly inhibited, in a dose-dependent manner, the survival of osteoclasts differentiated from RAW 264.7 cells and induced the apoptosis of osteoclasts. Treatment with (-)-epigallocatechin gallate resulted in DNA fragmentation and induced the activation of caspase-3 in RAW 264.7 cell-derived osteoclasts. Additional treatment with Z-VAD-FMK suppressed these effects of (-)-epigallocatechin gallate. Conclusion: From these findings, we could suggest that (-)-epigallocatechin gallate might prevent alveolar bone resorption by inhibiting osteoclast survival through the caspase-mediated apoptosis.

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