Anti-inflammatory Effects of KOTMIN13: A Mixed Herbal Medicine in LPS-stimulated RAW 264.7 Cells and Mouse Edema Models
| Autor: | Hwadong Lee, Eunkyung Lee, Na-Young Park, Hyo-Hyun Park, In-Hae Lee, Sun-Gun Kim, Jongkeun Choi, Eujin Lee, Kyu-Tae Jeong |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Nuclear Factor-Kappaβ (NF-kβ) p38 mitogen-activated protein kinases Pharmaceutical Science Inflammation Pharmacology Nitric oxide 03 medical and health sciences chemistry.chemical_compound Edema 12-O-tetradecanoylphorobol-13 aceate-induced ear edema Drug Discovery Medicine MAP (Mitogen-activated protein) Traditional medicine biology business.industry Interleukin Inflammatory mediators Nitric oxide synthase 030104 developmental biology chemistry carrageenan-induced paw edema biology.protein Tumor necrosis factor alpha Original Article medicine.symptom business |
| Zdroj: | Pharmacognosy Magazine |
| ISSN: | 0973-1296 |
| Popis: | Background: A Korean herbal medicine, KOTMIN13, composed of Inula japonica Thunberg, Trichosanthes kirilowii Maximowicz var. japonica kitamura, Peucedanum praeruptorum Dunn, and Allium macrostemon Bge, has been used for anti-allergic and anti-asthmatic treatment in oriental clinics, but its activity has not been investigated. Materials and Methods: To evaluate the anti-inflammatory activity of KOTMIN13 for in vitro study, LPS-stimulated RAW 264.7 cells were used to induce the production and expression of inflammatory mediators and its mechanisms. 12-O-Tetradecanoylphorobol-13 aceate (TPA)-induced ear edema and carrageenan-induced paw edema models were also used to evaluate the effect of KOTMIN13 on acute inflammation in vivo. Results: KOTMIN13 reduced the release of inflammatory mediators [nitric oxide, prostaglandin E2, interleukin (IL)-1β, and IL-6] and the protein expression of inducible nitric oxide synthase and cyclooxygenase-2 in LPS-stimulated RAW 264.7 cells. Mechanism studies showed the attenuation of LPS-induced NF-κB activation by KOTMIN13 via IκBα degradation abrogation and a subsequent decrease in nuclear p65 levels. Activation of mitogen-activated protein kinases (ERK, JNK, and p38) was also suppressed. Furthermore, KOTMIN13 ameliorated the development of TPA-induced ear edema and carrageenan-induced paw edema in acute inflammatory edema mouse models. Conclusion: Our study demonstrates that KOTMIN13 inhibits inflammatory mediators through the inhibitions of NF-κB and MAPK activities in LPS-induced RAW 264.7 cells, as well as acute inflammation in edema models, indicating that KOTMIN13 is an effective suppressor for anti-inflammatory activities. SUMMARY KOTMIN13 decrease the production of No, PGE2, and proinflammatory cytokine (TNF-∝, IL-1β,IL-6).KOTMIN13 Suppressed the degradation of NF-kβ and IKβα and the phosorylation of MAP Kinases.Topical application of KOTMIN13 reduced mouse ear edema.Oral administration of KOTMIN13 decreased carrageenan-induced paw edema. Abbreviations used: NO: nitric oxide; PGE2: prostaglandin E2; iNOS: inducible NO synthase; COX-2: cyclooxygenase-2; TNF-α: tumor necrosis factor-α; IL: interleukin; NF-κB: nuclear factor kappaB; MAPK: mitogen-activated protein kinases; ERK: extracellular signal regulated kinase; JNK: c-jun N terminal kinase; TPA: 12-O-tetradecanoylphorbol-13-acetate |
| Databáze: | OpenAIRE |
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