NDLI: Green tea catechin inhibits lipopolysaccharide-induced bone resorption in vivo.

Please wait, while we are loading the content...

Year: 2017 Volume: 52

Year: 2016 Volume: 51

Year: 2015 Volume: 50

Year: 2014 Volume: 49

Year: 2013 Volume: 48

Year: 2012 Volume: 47

Year: 2011 Volume: 46

Year: 2010 Volume: 45

Year: 2010 Volume: 45 Issue: 6

Year: 2010 Volume: 45 Issue: 5

Year: 2010 Volume: 45 Issue: 4

Year: 2010 Volume: 45 Issue: 3

Year: 2010 Volume: 45 Issue: 2

Year: 2010 Volume: 45 Issue: 1

Defining a visual marker of osteoprogenitor cells within the periodontium.

Effects of topical application of lipopolysaccharide and proteases on hepatic injury induced by high-cholesterol diet in rats.

A quinol peroxidase inhibitor prevents secretion of a leukotoxin from Aggregatibacter actinomycetemcomitans.

Periodontitis-associated up-regulation of systemic inflammatory mediator level may increase the risk of coronary heart disease.

Effect of matrix metalloproteinase-1 promoter genotype on interleukin-1beta-induced matrix metalloproteinase-1 production in human periodontal ligament cells.

A novel murine model for chronic inflammatory alveolar bone loss.

Preconditioning with Porphyromonas gingivalis lipopolysaccharide may confer cardioprotection and improve recovery of the electrically induced intracellular calcium transient during ischemia and reperfusion

Epidermal growth factor released from platelet-rich plasma promotes endothelial cell proliferation in vitro.

A multiplex immunoassay demonstrates reductions in gingival crevicular fluid cytokines following initial periodontal therapy.

Shosaikoto increases calprotectin expression in human oral epithelial cells.

Hydrogen sulfide induces apoptosis in human periodontium cells

Oral malodorous compound triggers mitochondrial-dependent apoptosis and causes genomic DNA damage in human gingival epithelial cells

Green tea catechin inhibits lipopolysaccharide-induced bone resorption in vivo.

Host beta-globin gene fragments in crevicular fluid as a biomarker in periodontal health and disease.

Immunohistochemical localization of elastin, fibrillins and microfibril-associated glycoprotein-1 in the developing periodontal ligament of the rat molar.

Effects of mechanical stimulation by a powered toothbrush on the healing of periodontal tissue in a rat model of periodontal disease.

The association of psychosocial factors and smoking with periodontal health in a community population.

Effect of cyclic mechanical loading on osteoclast recruitment in periodontal tissue.

Matrix metalloproteinase-3 gene polymorphism in renal transplant patients with gingival overgrowth.

Expression of receptor activator of nuclear factor kappaB ligand in ligature-induced periodontitis in osteoporotic and non-osteoporotic rats.

Systemic endotoxin levels in chronic indolent periodontal infections.

Year: 2009 Volume: 44

Year: 2008 Volume: 43

Year: 2007 Volume: 42

Year: 2006 Volume: 41

Year: 1996 Volume: 31

Green tea catechin inhibits lipopolysaccharide-induced bone resorption in vivo.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Nakamura, H. Ukai, T. Yoshimura, A. Kozuka, Y. Yoshioka, H. Yoshinaga, Y. Abe, Y. Hara, Y.
Description	Country affiliation: Japan Author Affiliation: Nakamura H ( Department of Periodontology, Unit of Translational Medicine, Course of Medical and Dental Sciences, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki, Japan.)
Abstract	BACKGROUND AND 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. MATERIAL AND 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. CONCLUSION: These results suggest that GTC suppresses LPS-induced bone resorption by inhibiting IL-1beta production or by directly inhibiting osteoclastogenesis.
File Format	HTM / HTML
ISSN	00223484
Issue Number	1
Volume Number	45
e-ISSN	16000765
Journal	Journal of Periodontal Research
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-02-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Dentistry Alveolar Bone Loss Prevention & Control Antioxidants Therapeutic Use Catechin Escherichia Coli Lipopolysaccharides Adverse Effects Animals Antigens, Cd14 Drug Effects Administration & Dosage Pharmacology Bone Marrow Cells Cho Cells Analogs & Derivatives Cell Count Cell Nucleus Cells, Cultured Cricetinae Cricetulus Dose-response Relationship, Drug Interleukin-1beta Interleukin-2 Receptor Alpha Subunit Macrophage Colony-stimulating Factor Macrophages Male Mice Mice, Inbred Balb C Nf-kappa B Osteoclasts Pathology Rank Ligand Tea Journal Article
Content Type	Text
Resource Type	Article
Subject	Periodontics

Central Library (ISO-9001:2015 Certified)
Indian Institute of Technology Kharagpur
Kharagpur, West Bengal, India | PIN - 721302

See location in the Map
03222 282435
Mail: support@ndl.gov.in

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in