Green tea catechin inhibits lipopolysaccharide-induced bone resorption in vivo.
OBJECTIVE
Bone resorption is positively regulated by receptor activator of nuclear factor-kappaB ligand (RANKL). Pro-inflammatory cytokines, such as interleukin (IL)-1beta, promote RANKL expression by stromal cells and osteoblasts. Green tea catechin (GTC) has beneficial effects on human health and has been reported to inhibit osteoclast formation in an in vitro co-culture system. However, there has been no investigation of the effect of GTC on periodontal bone resorption in vivo. We therefore investigated whether GTC has an inhibitory effect on lipopolysaccharide (LPS)-induced bone resorption.


METHODS
Escherichia coli (E. coli) LPS or LPS with GTC was injected a total of 10 times, once every 48 h, into the gingivae of BALB/c mice. Another group of mice, housed with free access to water containing GTC throughout the experimental period, were also injected with LPS in a similar manner.


RESULTS
The alveolar bone resorption and IL-1beta expression induced by LPS in gingival tissue were significantly decreased by injection or oral administration of GTC. Furthermore, when GTC was added to the medium, decreased responses to LPS were observed in CD14-expressing Chinese hamster ovary (CHO) reporter cells, which express CD25 through LPS-induced nuclear factor-kappaB (NF-kappaB) activation. These findings demonstrated that GTC inhibits nuclear translocation of NF-kappaB activated by LPS. In addition, osteoclasts were generated from mouse bone marrow macrophages cultured in a medium containing RANKL and macrophage colony-stimulating factor with or without GTC. The number of osteoclasts was decreased in dose-dependent manner when GTC was added to the culture medium.


CONCLUSIONS
These results suggest that GTC suppresses LPS-induced bone resorption by inhibiting IL-1beta production or by directly inhibiting osteoclastogenesis.
Nakamura
H
H
Department of Periodontology, Unit of Translational Medicine, Course of Medical and Dental Sciences, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki, Japan.
Ukai
T
T
Yoshimura
A
A
Kozuka
Y
Y
Yoshioka
H
H
Yoshinaga
Y
Y
Abe
Y
Y
Hara
Y
Y
D016301:Alveolar Bone Loss / Q000517:prevention & control*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D001854:Bone Marrow Cells / Q000187:drug effects; D016466:CHO Cells; D002392:Catechin / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use*; D002452:Cell Count; D002467:Cell Nucleus / Q000187:drug effects; D002478:Cells, Cultured; D006224:Cricetinae; D003412:Cricetulus; D004305:Dose-Response Relationship, Drug; D004926:Escherichia coli; D053583:Interleukin-1beta / Q000187:drug effects; D053645:Interleukin-2 Receptor alpha Subunit / Q000187:drug effects; D018950:Lipopolysaccharide Receptors / Q000187:drug effects; D008070:Lipopolysaccharides / Q000009:adverse effects*; D016173:Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000187:drug effects; D010010:Osteoclasts / Q000187:drug effects / Q000473:pathology; D053245:RANK Ligand / Q000494:pharmacology; D013662:Tea
D000975:Antioxidants; D053583:Interleukin-1beta; D053645:Interleukin-2 Receptor alpha Subunit; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D016328:NF-kappa B; D053245:RANK Ligand; D013662:Tea; D016173:Macrophage Colony-Stimulating Factor; D002392:Catechin; C062669:epicatechin gallate; C045651:epigallocatechin gallate; C057580:gallocatechol