Prunella vulgaris extract and rosmarinic acid suppress lipopolysaccharide-induced alteration in human gingival fibroblasts
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
19159670
DOI
10.1016/j.tiv.2008.12.021
PII: S0887-2333(08)00315-9
Knihovny.cz E-zdroje
- MeSH
- antagonismus léků MeSH
- antioxidancia analýza farmakologie MeSH
- cinnamáty analýza farmakologie MeSH
- depsidy analýza farmakologie MeSH
- fibroblasty účinky léků metabolismus patologie MeSH
- gingiva účinky léků metabolismus patologie MeSH
- glutathion metabolismus MeSH
- kultivované buňky MeSH
- kyselina rozmarýnová MeSH
- lidé MeSH
- lipopolysacharidy antagonisté a inhibitory toxicita MeSH
- oxidační stres účinky léků MeSH
- Prunella chemie MeSH
- reaktivní formy kyslíku metabolismus MeSH
- rostlinné extrakty farmakologie MeSH
- viabilita buněk účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antioxidancia MeSH
- cinnamáty MeSH
- depsidy MeSH
- glutathion MeSH
- kyselina rozmarýnová MeSH
- lipopolysacharidy MeSH
- reaktivní formy kyslíku MeSH
- rostlinné extrakty MeSH
Periodontitis is a chronic disease associated with inflammation of the tooth-supporting tissues. The inflammation is initiated by a group of gram-negative anaerobic bacteria. These express a number of irritating factors including a lipopolysaccharide (LPS), which plays a key role in periodontal disease development. Plant extracts with anti-inflammatory and anti-microbial properties have been shown to inhibit bacterial plaque formation and thus prevent chronic gingivitis. In this study we tested effects of Prunella vulgaris L. extract (PVE; 5, 10, 25microg/ml) and its component rosmarinic acid (RA; 1microg/ml) on LPS-induced oxidative damage and inflammation in human gingival fibroblasts. PVE and RA reduced reactive oxygen species (ROS) production, intracellular glutathione (GSH) depletion as well as lipid peroxidation in LPS-treated cells. Treatment with PVE and RA also inhibited LPS-induced up-regulation of interleukin 1beta (IL-1beta), interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and suppressed expression of inducible nitric oxide synthase (iNOS). The results indicate that PVE and RA are able to suppress LPS-induced biological changes in gingival fibroblasts. The effects of PVE and RA are presumably linked to their anti-inflammatory activities and thus use of PVE and RA may be relevant in modulating the inflammation process, including periodontal disease.
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