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Ozonated Sunflower Oil (OSO) alleviates inflammatory responses in oxazolone-induced atopic dermatitis (AD)-like mice and LPS- treated RAW 264.7 cells.
Journal of Microbiology and Biotechnology ( IF 2.8 ) Pub Date : 2024-01-12 , DOI: 10.4014/jmb.2310.10037
Su-Young Kim 1, 2 , Jung Ok Lee 1 , Sue Lee 1, 2 , Jihye Heo 1, 2 , Kyung-Hyun Cho 3 , Ashutosh Bahuguna 3 , Kwang-Ho Yoo 1 , Beom Joon Kim 1, 2
Affiliation  

Ozone, a highly reactive oxidant molecule, is widely used as a complementary therapy for various skin diseases, including wound healing, pressure ulcers, diabetic foot, and infections. However, there is limited research on the effectiveness of ozone for atopic dermatitis (AD). Ozonated sunflower oil (OSO) is an active ingredient obtained from partially ozonated sunflower oil (SO). OSO markedly reduced the LPS-induced increase in IL-1β and nitric oxide (NO) levels in RAW 264.7 mouse macrophage cells. Oxazolone (OXZ) was applied to hairless mice to induce AD-like skin symptoms and immune response. OSO significantly alleviated the OXZ-induced increases in the number of infiltrating mast cells, epidermal thickness, AD symptoms, thymic stromal lymphopoietin (TSLP), and filaggrin, as well as the serum levels of NO, IgE, IL-1β, and TNF-α. Furthermore, OSO inhibited the IL-4/STAT3/MAPK pathway and the expression of NF-κB. Our results suggest that OSO treatment could relieve AD-mediated skin damage through its anti-inflammatory and antioxidant activities. Therefore, it can be used as a therapeutic agent against AD-related skin diseases.

中文翻译:

臭氧化葵花籽油 (OSO) 可减轻恶唑酮诱导的特应性皮炎 (AD) 样小鼠和 LPS 处理的 RAW 264.7 细胞的炎症反应。

臭氧是一种高活性氧化剂分子,被广泛用作各种皮肤疾病的补充疗法,包括伤口愈合、压疮、糖尿病足和感染。然而,关于臭氧治疗特应性皮炎 (AD) 有效性的研究有限。臭氧化葵花籽油 (OSO) 是从部分臭氧化葵花籽油 (SO) 中提取的活性成分。OSO 显着降低了 LPS 诱导的 RAW 264.7 小鼠巨噬细胞中 IL-1β 和一氧化氮 (NO) 水平的增加。恶唑酮 (OXZ) 被应用于无毛小鼠以诱导 AD 样皮肤症状和免疫反应。OSO 显着减轻 OXZ 诱导的浸润肥大细胞数量、表皮厚度、AD 症状、胸腺基质淋巴细胞生成素 (TSLP) 和聚丝蛋白以及 NO、IgE、IL-1β 和 TNF-α 血清水平的增加。 α。此外,OSO 抑制 IL-4/STAT3/MAPK 通路和 NF-κB 的表达。我们的结果表明,OSO 治疗可以通过其抗炎和抗氧化活性减轻 AD 介导的皮肤损伤。因此,它可以用作AD相关皮肤病的治疗剂。
更新日期:2024-01-12
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