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Anti-Inflammatory Effect of Titrated Extract of Centella asiatica in Phthalic Anhydride-Induced Allergic Dermatitis Animal Model.

Artikel i vetenskaplig tidskrift
Författare Ju Ho Park
Ji Yeon Choi
Dong Ju Son
Eun Kyung Park
Min Jong Song
Mats Hellström
Jin Tae Hong
Publicerad i International journal of molecular sciences
Volym 18
Nummer/häfte 4
ISSN 1422-0067
Publiceringsår 2017
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för obstetrik och gynekologi
Språk en
Länkar dx.doi.org/10.3390/ijms18040738
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Anti-Inflammatory Agents, administration & dosage, pharmacology, therapeutic use, Cell Line, Cyclooxygenase 2, metabolism, Dermatitis, Allergic Contact, drug therapy, etiology, Interleukins, blood, Macrophages, drug effects, metabolism, Mice, NF-kappa B, metabolism, Nitric Oxide Synthase Type II, metabolism, Phthalic Anhydrides, toxicity, Skin, drug effects, metabolism, Triterpenes, administration & dosage, pharmacology, therapeutic use, Tumor Necrosis Factor-alpha, blood
Ämneskategorier Farmakologi och toxikologi, Medicinska grundvetenskaper

Sammanfattning

Centella asiatica has potent antioxidant and anti-inflammatory properties. However, its anti-dermatitic effect has not yet been reported. In this study, we investigated the anti-dermatitic effects of titrated extract of Centella asiatica (TECA) in a phthalic anhydride (PA)-induced atopic dermatitis (AD) animal model as well as in vitro model. An AD-like lesion was induced by the topical application of five percent PA to the dorsal skin or ear of Hos:HR-1 mouse. After AD induction, 100 μL of 0.2% and 0.4% of TECA (40 μg or 80 μg/cm²) was spread on the dorsum of the ear or back skin three times a week for four weeks. We evaluated dermatitis severity, histopathological changes and changes in protein expression by Western blotting for inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and NF-κB activity, which were determined by electromobility shift assay (EMSA). We also measured TNF-α, IL-1β, IL-6, and IgE concentration in the blood of AD mice by enzyme-linked immunosorbent assay (ELISA). TECA treatment attenuated the development of PA-induced atopic dermatitis. Histological analysis showed that TECA inhibited hyperkeratosis, mast cells and infiltration of inflammatory cells. TECA treatment inhibited expression of iNOS and COX-2, and NF-κB activity as well as the release of TNF-α, IL-1β, IL-6, and IgE. In addition, TECA (1, 2, 5 μg/mL) potently inhibited Lipopolysaccharide (LPS) (1 μg/mL)-induced NO production, expression of iNOS and COX-2, and NF-κB DNA binding activities in RAW264.7 macrophage cells. Our data demonstrated that TECA could be a promising agent for AD by inhibition of NF-κB signaling.

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