Anti-inflammatory effect of bee venom in phthalic anhydride-induced atopic dermatitis animal model.
Yu Jin LeeMyung Jin OhDong Hun LeeYong Sun LeeJiin LeeDeok-Hyun KimCheol-Hoon ChoiMin Jong SongHo Sueb SongJin Tae HongPublished in: Inflammopharmacology (2019)
Globally, many people have been affected with atopic dermatitis (AD), a chronic inflammatory skin disease. AD is associated with multiple factors such as genetic, inflammatory, and immune factors. Bee venom (BV) is now widely used for the treatment of several inflammatory diseases. However, its effect on 5% phthalic anhydride (PA)-induced AD has not been reported yet. We investigated the anti-inflammatory and anti-AD effects of BV in a PA-induced animal model of AD. Balb/c mice were treated with topical application of 5% PA to the dorsal skin and ears for induction of AD. After 24 h, BV was applied on the back and ear skin of the mice three times a week for 4 weeks. BV treatment significantly reduced the PA-induced AD clinical score, back and ear epidermal thickness, as well as IgE level and infiltration of immune cells in the skin tissues compared to those of control mice. The levels of inflammatory cytokines in the serum were significantly decreased in BV-treated group compared to PA-treated group. In addition, BV inhibited the expression of iNOS and COX-2 as well as the activation of mitogen-activated protein kinase (MAPK) and NF-ҡB induced by PA in the skin tissues. We also found that BV abrogated the lipopolysaccharide or TNF-α/IFN-γ-induced NO production, expression of iNOS and COX-2, as well as MAPK and NF-ҡB signaling pathway in RAW 264.7 and HaCaT cells. These results suggest that BV may be a potential therapeutic macromolecule for the treatment of AD.
Keyphrases
- lps induced
- signaling pathway
- lipopolysaccharide induced
- oxidative stress
- diabetic rats
- high glucose
- inflammatory response
- pi k akt
- induced apoptosis
- wound healing
- soft tissue
- anti inflammatory
- drug induced
- type diabetes
- clinical trial
- randomized controlled trial
- immune response
- combination therapy
- toll like receptor
- dna methylation
- nitric oxide synthase
- endothelial cells
- copy number
- neuropathic pain
- newly diagnosed
- high resolution
- cell cycle arrest
- endoplasmic reticulum stress
- tyrosine kinase
- genome wide
- stress induced
- spinal cord injury
- gestational age