Evaluation of the Anti-Atopic Dermatitis Effects of α-Boswellic Acid on Tnf-α/Ifn-γ-Stimulated HaCat Cells and DNCB-Induced BALB/c Mice.
Ya-Chu TsaiHsun-Hao ChangSheng-Chieh ChouThomas W ChuYu-Jou HsuChien-Yu HsiaoYuan-Hsin LoNan-Lin WuDer-Chen ChangChi-Feng HungPublished in: International journal of molecular sciences (2022)
Boswellic acids, triterpenoids derived from the genus Boswellia (Burseraceae), are known for their anti-inflammatory and anti-tumor efficacy. Atopic dermatitis is a chronic, non-infectious inflammatory skin disease. However, the effects of α-boswellic acid on atopic dermatitis have not been studied. Therefore, in this study we examined the expression level of pro-inflammatory cytokines, histopathological analysis, and physiological data from BALB/c mice with atopic-like dermatitis induced by 2,4-dinitrochlorobenzene and TNF-α/IFN-γ-stimulated HaCaT cells to better understand the agent's anti-atopic dermatitis efficacy. First, we found that α-boswellic reduced the epidermal thickening, mast cell numbers, and dermal infiltration of 2,4-dinitrochlorobenzene-induced atopic-like dermatitis in BALB/c mice. Furthermore, we also found that α-boswellic acid can restore transepidermal water loss and skin reddening in mice. In human keratinocytes inflamed by TNF-α/IFN-γ, α-boswellic acid inhibited MAP kinase activation and showed a reduction in NF-κB nuclear translocation. Finally, α-boswellic acid can reduce the expression level of cytokines (IL-1β, IL-6, and IL-8) following the stimulation of TNF-α/IFN-γ in HaCaT cells. Taken together, our study suggests that α-boswellic acids are a potential component for the development of anti-atopic dermatitis drugs.
Keyphrases
- atopic dermatitis
- induced apoptosis
- rheumatoid arthritis
- cell cycle arrest
- dendritic cells
- high fat diet induced
- immune response
- anti inflammatory
- poor prognosis
- signaling pathway
- wound healing
- oxidative stress
- high glucose
- endothelial cells
- cell death
- endoplasmic reticulum stress
- diabetic rats
- risk assessment
- cell proliferation
- big data
- tyrosine kinase
- lps induced
- toll like receptor
- inflammatory response
- human health
- skeletal muscle
- binding protein
- climate change
- protein kinase