galangin and Chronic-Disease

Galangin is a member of the flavonol class of flavonoids having anti-inflammatory and anti-oxidative potential. Previously we reported the inhibitory effect of galangin on the mast cell-mediated allergic inflammation. For incremental research, we investigated the effects of galangin on atopic dermatitis (AD)-like skin lesions and underlying mechanisms of action. We established an atopic dermatitis model in BALB/c mice by repeated local exposure of house dust mite (Dermatophagoides farinae) extract (DFE) and 2,4-dinitrochlorobenzene (DNCB) to the ears. Repeated alternative treatment of DFE/DNCB caused AD-like skin lesions. Topical application of galangin reduced AD symptoms based on ear thickness and histopathological analysis, in addition to serum IgE and IgG2a levels. Galangin inhibited mast cell infiltration into the ear and serum histamine level. Galangin suppressed DFE/DNCB-induced expression of interleukin (IL)-4, IL-5, IL-13, IL-31, IL-32, and interferon (IFN)-γ in the ear tissue. To define the underlying mechanisms of action, tumor necrosis factor-α/IFN-γ-activated human keratinocytes (HaCaT) model was used. Galangin significantly inhibited the expression of cytokines and chemokine by the down-regulation of nuclear factor-κB and mitogen-activated protein kinases in HaCaT cells. Taken together, the results demonstrate that galangin inhibited AD-like symptoms, suggesting that galangin might be a candidate for the treatment of AD.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents; Antigens, Dermatophagoides; Antioxidants; Cell Survival; Cells, Cultured; Chronic Disease; Dermatitis, Atopic; Dinitrochlorobenzene; Down-Regulation; Female; Flavonoids; Histamine; Humans; Immunoglobulins; Interferon-gamma; Interleukins; Keratinocytes; Mast Cells; Mice; Mice, Inbred BALB C; Mitogen-Activated Protein Kinases; NF-kappa B; Tumor Necrosis Factor-alpha

Two ethanolic propolis extracts (EPE) with and without the caffeic acid phenethyl ester (CAPE), CAPE and galangin (major components of propolis) were investigated for anti-inflammatory activity in rats using carrageenin foot oedema, carrageenin pleurisy and adjuvant arthritis. In our experiments, EPE with CAPE and CAPE alone significantly inhibited carrageenin oedema, carrageenin pleurisy and adjuvant arthritis. In contrast EPE without CAPE and galangin did not exhibit anti-inflammatory effects in acute and chronic inflammation. These results suggest that the anti-inflammatory activity of propolis is due to CAPE.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents; Arthritis; Caffeic Acids; Carrageenan; Cell Division; Chronic Disease; Edema; Flavonoids; Male; Phenylethyl Alcohol; Phytotherapy; Plant Extracts; Pleurisy; Propolis; Rats; Rats, Inbred Lew; Rats, Wistar; T-Lymphocytes; Time Factors