Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu 41062, Korea.
Int J Mol Sci. 2022 Jan 5;23(1):553. doi: 10.3390/ijms23010553.
Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with a type 2 T helper cell (Th2) immune response. The extract (CHD) is used in traditional Southeast Asian medicine; however, its beneficial effects on AD remain uninvestigated. Therefore, we investigated the therapeutic effects of CHD in 2,4-dinitrochlorobenzene (DNCB)-induced BALB/c mice and tumor necrosis factor (TNF)-α- and interferon gamma (IFN)-γ-stimulated HaCaT cells. We evaluated immune cell infiltration, skin thickness, and the serum IgE and TNF-α levels in DNCB-induced AD mice. Moreover, we measured the expression levels of pro-inflammatory cytokines, mitogen-activated protein kinase (MAPK), and the nuclear factor-kappa B (NF-κB) in the mice dorsal skin. We also studied the effect of CHD on the translocation of NF-κB p65 and inflammatory chemokines in HaCaT cells. Our in vivo results revealed that CHD reduced the dermis and epidermis thicknesses and inhibited immune cell infiltration. Furthermore, it suppressed the proinflammatory cytokine expression and MAPK and NF-κB phosphorylations in the skin tissue and decreased serum IgE and TNF-α levels. In vitro results indicated that CHD downregulated inflammatory chemokines and blocked NF-κB p65 translocation. Thus, we deduced that CHD is a potential drug candidate for AD treatment.
特应性皮炎（AD）是一种与 2 型辅助性 T 细胞（Th2）免疫反应相关的慢性炎症性皮肤病。提取物（CHD）用于传统的东南亚医学；然而，其对 AD 的有益作用仍未得到研究。因此，我们研究了 CHD 在 2,4-二硝基氯苯（DNCB）诱导的 BALB/c 小鼠和肿瘤坏死因子（TNF）-α和干扰素γ（IFN）-γ刺激的 HaCaT 细胞中的治疗作用。我们评估了 DNCB 诱导的 AD 小鼠中免疫细胞浸润、皮肤厚度以及血清 IgE 和 TNF-α水平。此外，我们测量了小鼠背部皮肤中促炎细胞因子、丝裂原活化蛋白激酶（MAPK）和核因子-κB（NF-κB）的表达水平。我们还研究了 CHD 对 HaCaT 细胞中 NF-κB p65 和炎症趋化因子易位的影响。我们的体内结果表明，CHD 降低了真皮和表皮厚度并抑制了免疫细胞浸润。此外，它还抑制了皮肤组织中促炎细胞因子的表达以及 MAPK 和 NF-κB 的磷酸化，并降低了血清 IgE 和 TNF-α水平。体外结果表明，CHD 下调了炎症趋化因子并阻断了 NF-κB p65 易位。因此，我们推断 CHD 是治疗 AD 的潜在候选药物。
