Oral supplementation with p-coumaric acid protects mice against diabetes-associated spontaneous destruction of periodontal tissue.


Journal

Journal of periodontal research
ISSN: 1600-0765
Titre abrégé: J Periodontal Res
Pays: United States
ID NLM: 0055107

Informations de publication

Date de publication:
Dec 2019
Historique:
received: 25 11 2018
revised: 09 04 2019
accepted: 09 06 2019
pubmed: 23 7 2019
medline: 16 1 2020
entrez: 23 7 2019
Statut: ppublish

Résumé

Dietary bioactive materials having anti-inflammatory and antioxidant potentials are able to inhibit diabetes-associated periodontal complications. Although numerous studies indicate that administration of p-coumaric acid (p-CA) ameliorates diabetes and diabetes-related complications, the roles of p-CA on periodontal tissue destruction in diabetic mice and the possible mechanisms therein are not completely understood. In this study, we evaluated whether supplementation with p-CA protects mice against diabetes-associated spontaneous periodontal destruction and also explored the associated mechanism therein using in vivo and in vitro experimental systems. C57BL/6 male mice were divided into sham, streptozotocin (STZ), and STZ+CA groups (n = 5/group). Sham group was intraperitoneally injected with sodium buffer, whereas other two groups were injected with the buffer containing 160 mg/kg of STZ. STZ-induced diabetic mice received oral gavage with p-CA (50 mg/kg) (STZ+CA group) or with buffer only (STZ group) daily for 6 weeks. The effect of p-CA on diabetes-associated spontaneous periodontal destruction was evaluated using μCT analysis, hematoxylin and eosin staining, tartrate-resistant acid phosphatase staining, and immunohistochemical staining methods. The efficacies of p-CA on cell proliferation, osteoblast differentiation, reactive oxygen species (ROS) accumulation, and antioxidant-related marker expression were examined using human periodontal ligament fibroblasts (hPLFs) cultured under high glucose condition. Streptozotocin group exhibited periodontal tissue destruction along with increased inflammation, oxidative stress, and osteoclast formation, as well as with decreased osteogenesis. However, oral administration with p-CA protected mice against STZ-induced periodontal destruction by inhibiting inflammation and osteoclastic activation. STZ+CA group also showed higher expression of antioxidant and osteogenic markers in periodontal tissue than did STZ group. Treatment with high glucose concentration (30 mmol/L) impaired proliferation and osteoblast differentiation of hPLFs along with cellular ROS accumulation, whereas these impairments were almost completely disappeared by supplementation with p-CA. These findings demonstrate that supplementation with p-CA inhibits diabetes-associated spontaneous destruction of periodontal tissue by enhancing anti-inflammatory, anti-osteoclastogenic, and antioxidant defense systems in STZ-treated mice.

Identifiants

pubmed: 31328274
doi: 10.1111/jre.12678
doi:

Substances chimiques

Antioxidants 0
Coumaric Acids 0
Propionates 0
Streptozocin 5W494URQ81
p-coumaric acid IBS9D1EU3J

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

690-701

Subventions

Organisme : Biomedical Research Institute of Chonbuk National University Hospital
ID : CHU2017-0045
Organisme : Basic Science Research Program through the National Research Foundation (NRF) funded by the Ministry of Science, ICT and future Planning
ID : 2016R1A2A2A05921669
Organisme : Basic Science Research Program through the National Research Foundation (NRF) funded by the Ministry of Science, ICT and future Planning
ID : 2017R1A2B4009269
Organisme : Ministry of Education
ID : 2018R1D1A1B07047162
Organisme : Ministry of Education
ID : 2018R1D1A1B07046563
Organisme : RDA, Ministry of Agriculture and Forestry
ID : PJ01339402

Informations de copyright

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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Auteurs

Govinda Bhattarai (G)

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Korea.

Chang-Ki Min (CK)

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Korea.

Young-Mi Jeon (YM)

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Korea.
Research Institute of Clinical Medicine of Chonbuk National University, Jeonju, Korea.

Rajendra Bashyal (R)

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Korea.

Sher B Poudel (SB)

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Korea.

Sung-Ho Kook (SH)

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Korea.
Department of Bioactive Material Sciences, Research Center of Bioactive Materials, Chonbuk National University, Jeonju, Korea.

Jeong-Chae Lee (JC)

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Korea.
Research Institute of Clinical Medicine of Chonbuk National University, Jeonju, Korea.
Department of Bioactive Material Sciences, Research Center of Bioactive Materials, Chonbuk National University, Jeonju, Korea.

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