J of Periodontal Research

1992

DOI: 10.1111/j.1600-0765.1992.tb01829.x

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Flurbiprofen effect on gingival crevicular fluid prostaglandin and thromboxane levels in humans

Matthew Abramson

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Steven Offenbacher

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et al.

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Effects Of Nsaids Administration On the Development Of Gingi1

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Cited by 28 publications

(19 citation statements)

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“…2). And several clinical studies indicated that the concentration of PGE 2 in gingival crevicular fluid (GCF) is increased in periodontal disease 23) and is decreased by the administration of NSAIDs such as oral administration with flurbiprofen 24) and mouse wash with ketrolac. 25) Considering the facts that both NSAIDs and TJ-9 suppress PGE 2 production, it is possible that administration of TJ-9 also decreases PGE 2 concentration in GCF and results in the improvement of gingival inflammation.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of a Kampo Medicine, Shosaikoto, on Inflammatory Responses in LPS-Treated Human Gingival Fibroblasts

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et al. 2008

Biological & Pharmaceutical Bulletin

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In the present study, we investigated the anti-inflammatory effects of a Kampo medicine Shosaikoto (TJ-9) using in vitro periodontal disease model, in which human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) from Porphyromonas gingivalis (PgLPS) produce IL-6, IL-8 and prostaglandin E 2 (PGE 2 ). Treatment with PgLPS (10 ng/ml), TJ-9 (up to 1 mg/ml) and their combinations for 24 h did not affect the viability of HGFs. Moreover, TJ-9 did not alter LPS-induced IL-6 and IL-8 productions. However, TJ-9 significantly suppressed LPS-induced PGE 2 production in a dose-dependent manner but TJ-9 alone did not affect basal PGE 2 level. Western blotting demonstrated that TJ-9 decreased cyclooxygenase-2 (COX-2) expression in a dosedependent manner but not phospholipase A 2 . Moreover, TJ-9 selectively and dose-dependently inhibited COX-2 activity. These results suggest that TJ-9 decreased PGE 2 production by inhibition of both COX-2 expression and activity and that TJ-9 may be useful to improve gingival inflammation in periodontal disease.

“…2). And several clinical studies indicated that the concentration of PGE 2 in gingival crevicular fluid (GCF) is increased in periodontal disease 23) and is decreased by the administration of NSAIDs such as oral administration with flurbiprofen 24) and mouse wash with ketrolac. 25) Considering the facts that both NSAIDs and TJ-9 suppress PGE 2 production, it is possible that administration of TJ-9 also decreases PGE 2 concentration in GCF and results in the improvement of gingival inflammation.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of a Kampo Medicine, Shosaikoto, on Inflammatory Responses in LPS-Treated Human Gingival Fibroblasts

¹

,

²

,

³

et al. 2008

Biological & Pharmaceutical Bulletin

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In the present study, we investigated the anti-inflammatory effects of a Kampo medicine Shosaikoto (TJ-9) using in vitro periodontal disease model, in which human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) from Porphyromonas gingivalis (PgLPS) produce IL-6, IL-8 and prostaglandin E 2 (PGE 2 ). Treatment with PgLPS (10 ng/ml), TJ-9 (up to 1 mg/ml) and their combinations for 24 h did not affect the viability of HGFs. Moreover, TJ-9 did not alter LPS-induced IL-6 and IL-8 productions. However, TJ-9 significantly suppressed LPS-induced PGE 2 production in a dose-dependent manner but TJ-9 alone did not affect basal PGE 2 level. Western blotting demonstrated that TJ-9 decreased cyclooxygenase-2 (COX-2) expression in a dosedependent manner but not phospholipase A 2 . Moreover, TJ-9 selectively and dose-dependently inhibited COX-2 activity. These results suggest that TJ-9 decreased PGE 2 production by inhibition of both COX-2 expression and activity and that TJ-9 may be useful to improve gingival inflammation in periodontal disease.

“…And several clinical studies indicated that the concentration of PGE 2 in gingival crevicular fluid (GCF) is increased in periodontal disease 33) and is decreased by oral administration or mouse wash of NSAIDs. 34,35) Considering the facts that both NSAIDs and Orento suppress PGE 2 production, it is possible that administration of Orento also decreases PGE 2 concentration in GCF and results in the improvement of gingival inflammation. Therefore, Orento may be useful for the improvement of gingival inflammation in periodontal disease.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of a Kampo Medicine, Orento on Inflammatory Responses in Lipopolysaccharide Treated Human Gingival Fibroblasts

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,

²

,

³

et al. 2010

Biological & Pharmaceutical Bulletin

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“…And several clinical studies indicated that the concentration of PGE 2 in gingival crevicular fluid (GCF) is increased in periodontal disease 28) and is decreased by oral administration or mouse wash of NSAIDs 29,30) .…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of a Kampo Medicine, Hangeshashinto on Inflammatory Responses in Lipopolysaccharide-Treated Human Gingival Fibroblasts

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,

²

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³

et al. 2010

J. Hard Tissue Biology.

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In the present study, we investigated the effects of a Kampo medicine hangeshashinto (TJ-14) on the production of prostaglandin E 2 (PGE 2 ), interleukin (IL)-6 and IL-8 by human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) from Porphyromonas gingivalis. HGFs proliferation was dose-dependently decreased with hangeshashinto at days 3 and 7. However, treatment with LPS (10 ng/ml), hangeshashinto (up to 1 mg/ml) and their combinations for 24 h did not affect the viability of HGFs. Hangeshashinto dose-dependently suppressed LPS-induced PGE 2 production but did not alter basal PGE 2 level. Hangeshashinto weakly decreased LPS-induced IL-6 and IL-8 productions. Hangeshashinto decreased cyclooxygenase (COX)-1 and COX-2 activities to approximately 60% at 1 mg/ml. Hangeshashinto decreased cytoplasmic phospholipase A 2 (cPLA 2 ) expression and LPS-induced COX-2 expression but not affected annexin1 expression. Hangeshashinto weakly suppressed LPS-induced extracellular signal-regulated kinase (ERK) phosphorylation, which is known to lead to ERK activation and cPLA 2 phosphorylation. These results suggest that hangeshashinto decreased PGE 2 production by (1) suppression of cPLA 2 and LPS-induced COX-2 expression, and to a lesser extent, (2) inhibition of COX-2 activity and (3) inhibition of cPLA 2 phosphorylation and its activation via inhibition of ERK phosphorylation. Moreover, it is also suggested that hangeshashinto may be useful to improve gingival inflammation in periodontal disease.

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