| Literature DB >> 24361550 |
Hui-Hun Kim1, Seung-Bin Park1, Soyoung Lee1, Taeg Kyu Kwon2, Tae-Yong Shin3, Pil-Hoon Park4, Seung-Ho Lee4, Sang-Hyun Kim5.
Abstract
A great number of people are suffering from allergic inflammatory disease such as asthma, atopic dermatitis, and sinusitis. Therefore discovery of drugs for the treatment of these diseases is an important subject in human health. Putranjivain A (PJA), member of ellagitannin, is known to possess beneficial effects including anti-cancer and anti-viral activities. The aim of the present study was to elucidate whether PJA modulates the allergic inflammatory reaction and to study its possible mechanisms of action using mast cell-based in vitro and in vivo models. The study was performed in anaphylaxis mouse model and cultured mast cells. PJA inhibited the expression of pro-inflammatory cytokines in immunoglobulin E-stimulated mast cells. PJA reduced this expression by inhibiting nuclear factor (NF)-κB and nuclear factor of activated T cell. The oral administration of PJA reduced systemic and cutaneous anaphylaxis, the release of serum histamine, and the expression of the histamine H1 receptor. In addition, PJA attenuated the activation of mast cells. PJA inhibited the release of histamine from various types of mast cells by the suppression of intracellular calcium. The inhibitory activity of PJA on the allergic reaction was similar to that of disodium cromoglycate, a known anti-allergic drug. These results suggest that PJA can facilitate the prevention or treatment of allergic inflammatory diseases mediated by mast cells.Entities:
Keywords: Allergic inflammation; DNP; HMC; Histamine; Mast cells; NF-κB; NFAT; PCA; PMA; Putranjivain A; RBL; dinitrophenyl; human mast cell; nuclear factor of activated T cell; passive cutaneous anaphylaxis; phorbol 12-myristate 13-acetate; rat basophilic leukemia
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Year: 2013 PMID: 24361550 DOI: 10.1016/j.taap.2013.12.006
Source DB: PubMed Journal: Toxicol Appl Pharmacol ISSN: 0041-008X Impact factor: 4.219