Department of Biotechnology, Yonsei University, Seoul, South Korea.
Department of Biomaterials Science and Engineering, Yonsei University, Seoul, South Korea.
Life Sci. 2014 Mar 28;100(1):45-54. doi: 10.1016/j.lfs.2014.01.076. Epub 2014 Feb 11.
Panduratin A isolated from Boesenbergia pandurata (Roxb.) has been reported to have antioxidant, anti-inflammatory, and anti-allergic activities. However, the effect of panduratin A on atopic dermatitis (AD) has not been studied. In the present study, we investigated the efficacy of panduratin A, an activator of peroxisome proliferator-activated receptors (PPAR) α/δ, using oxazolone-induced AD-like model in hairless mice.
To determine PPARα/δ activation of panduratin A, HaCaT, Hs68, and COS-7 cells were treated with panduratin A, then PPARα/δ and PPAR response element (PPRE) activities were assessed with a reporter gene assay. For the in vivo study, oral administration of panduratin A was performed for 4weeks, with oxazolone treatment every other day. The efficacy of panduratin A on parameters of oxazolone-induced AD was assessed physiologically, morphologically, and immunologically.
Panduratin A increased PPARα/δ and PPRE activation both in vitro and in vivo. Panduratin A attenuated dermatitis-associated barrier damage as demonstrated by transepidermal water loss, erythema, and filaggrin expression. Furthermore, infiltration of inflammatory cells and epidermal thickness in the skin were decreased. Panduratin A decreased serum immunoglobulin (Ig) E and interleukin-4 levels but increased IgG2a and interferon-γ levels. In addition, panduratin A decreased inflammation-associated molecules in the skin. Panduratin A also decreased Th2-associated molecules and increased Th1/regulatory T cell (Treg)-associated molecules in the spleen.
Panduratin A showed a beneficial effect on AD by modulating Th1/Th2/Treg-associated immune response and is a potential candidate for treating AD.
从蓬莪术（Boesenbergia pandurata（Roxb.））中分离出的蓬莪定 A 已被报道具有抗氧化、抗炎和抗过敏活性。然而，蓬莪定 A 对特应性皮炎（AD）的影响尚未得到研究。在本研究中，我们使用无毛小鼠的氧化唑诱导的 AD 样模型研究了蓬莪定 A（过氧化物酶体增殖物激活受体（PPAR）α/δ 的激活剂）的功效。
为了确定蓬莪定 A 对 PPARα/δ 的激活作用，用蓬莪定 A 处理 HaCaT、Hs68 和 COS-7 细胞，然后用报告基因检测法评估 PPARα/δ 和 PPAR 反应元件（PPRE）的活性。在体内研究中，用蓬莪定 A 进行口服给药 4 周，每隔一天用氧化唑处理。通过生理、形态和免疫学评估蓬莪定 A 对氧化唑诱导的 AD 参数的疗效。
蓬莪定 A 体内外均能增加 PPARα/δ 和 PPRE 的激活。蓬莪定 A 减轻了与皮炎相关的屏障损伤，表现为经表皮水分流失、红斑和丝聚蛋白表达增加。此外，皮肤中炎症细胞的浸润和表皮厚度减少。蓬莪定 A 降低了血清免疫球蛋白（Ig）E 和白细胞介素-4 水平，但增加了 IgG2a 和干扰素-γ 水平。此外，蓬莪定 A 降低了皮肤中与炎症相关的分子。蓬莪定 A 还降低了脾脏中与 Th2 相关的分子，并增加了与 Th1/调节性 T 细胞（Treg）相关的分子。
蓬莪定 A 通过调节 Th1/Th2/Treg 相关免疫反应对 AD 具有有益作用，是治疗 AD 的潜在候选药物。
