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.

中文翻译：

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蜂毒在邻苯二甲酸酐诱发的特应性皮炎动物模型中的抗炎作用。

在全球范围内，许多人都患有特应性皮炎（AD），这是一种慢性炎症性皮肤病。AD与多种因素相关，例如遗传，炎症和免疫因素。蜂毒（BV）现在被广泛用于治疗几种炎症性疾病。然而，尚未报道其对5％邻苯二甲酸酐（PA）诱导的AD的作用。我们在PA诱导的AD动物模型中研究了BV的抗炎和抗AD作用。Balb / c小鼠通过在背部皮肤和耳朵局部应用5％PA诱导AD的治疗。24小时后，将BV每周3次施用于小鼠的背部和耳朵皮肤，持续4周。BV治疗可显着降低PA诱发的AD临床评分，背部和耳朵的表皮厚度，以及与对照组小鼠相比，皮肤组织中免疫细胞的IgE水平和浸润。与PA治疗组相比，BV治疗组的血清炎症细胞因子水平明显降低。此外，BV抑制了皮肤组织中PA诱导的iNOS和COX-2的表达以及丝裂原活化蛋白激酶（MAPK）和NF-ҡB的活化。我们还发现BV消除了脂多糖或TNF-α/IFN-γ诱导的NO产生，iNOS和COX-2的表达以及RAW 264.7和HaCaT细胞中的MAPK和NF-ҡB信号通路。这些结果表明，BV可能是用于治疗AD的潜在治疗性大分子。与PA治疗组相比，BV治疗组的血清炎性细胞因子水平明显降低。此外，BV抑制了皮肤组织中PA诱导的iNOS和COX-2的表达以及丝裂原活化蛋白激酶（MAPK）和NF-ҡB的活化。我们还发现BV消除了脂多糖或TNF-α/IFN-γ诱导的NO产生，iNOS和COX-2的表达以及RAW 264.7和HaCaT细胞中的MAPK和NF-ҡB信号通路。这些结果表明，BV可能是用于治疗AD的潜在治疗性大分子。与PA治疗组相比，BV治疗组的血清炎性细胞因子水平明显降低。此外，BV抑制了皮肤组织中PA诱导的iNOS和COX-2的表达以及丝裂原活化蛋白激酶（MAPK）和NF-ҡB的活化。我们还发现BV消除了脂多糖或TNF-α/IFN-γ诱导的NO产生，iNOS和COX-2的表达以及RAW 264.7和HaCaT细胞中的MAPK和NF-ҡB信号通路。这些结果表明，BV可能是用于治疗AD的潜在治疗性大分子。我们还发现BV消除了脂多糖或TNF-α/IFN-γ诱导的NO产生，iNOS和COX-2的表达以及RAW 264.7和HaCaT细胞中的MAPK和NF-ҡB信号通路。这些结果表明，BV可能是用于治疗AD的潜在治疗性大分子。我们还发现BV消除了脂多糖或TNF-α/IFN-γ诱导的NO产生，iNOS和COX-2的表达以及RAW 264.7和HaCaT细胞中的MAPK和NF-ҡB信号通路。这些结果表明，BV可能是用于治疗AD的潜在治疗性大分子。