CMRI, Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea.
Department of Nursing, Nambu University, Gwangju 506-706, Republic of Korea.
Int J Mol Med. 2017 Aug;40(2):505-511. doi: 10.3892/ijmm.2017.3017. Epub 2017 Jun 12.
Atopic dermatitis (AD) is a common chronic inflammatory skin disease, affecting 10-20% of individuals worldwide. Therefore, the discovery of drugs for treating AD is an attractive subject and important to human health. Diospyros kaki and Diospyros kaki (D. kaki) folium exert beneficial effects on allergic inflammation. However, the effect of D. kaki calyx on AD remains elusive. The present study evaluated the effects of an aqueous extract of D. kaki calyx (AEDKC) on AD-like skin lesions using mouse and keratinocyte models. We used a mouse AD model by the repeated skin exposure of house dust mite extract [Dermatophagoides farinae extract (DFE)] and 2,4-dinitrochlorobenzene (DNCB) to the ears. In addition, to determine the underlying mechanism of its operation, tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)-activated keratinocytes (HaCaT) were used. Oral administration of AEDKC decreased AD-like skin lesions, as demonstrated by the reduced ear thickness, serum immunoglobulin E (IgE), DFE-specific IgE, IgG2a, histamine level and inflammatory cell infiltration. AEDKC inhibited the expression of pro-inflammatory cytokines and a chemokine via downregulation of nuclear factor-κB and signal transducer and activator of transcription 1 in HaCaT cells. On examination of the AD-related factors in vivo and in vitro, it was confirmed that AEDKC decreased AD-like skin lesions. Taken together, the results suggest that AEDKC is a potential drug candidate for the treatment of AD.
特应性皮炎(AD)是一种常见的慢性炎症性皮肤病,影响全球 10-20%的个体。因此,发现治疗 AD 的药物是一个有吸引力的课题,对人类健康很重要。柿和柿叶对过敏炎症有有益的作用。然而,柿蒂对 AD 的影响尚不清楚。本研究采用小鼠和角质形成细胞模型评价柿蒂水提物(AEDKC)对 AD 样皮肤损伤的作用。我们采用重复皮肤暴露于屋尘螨提取物(DFE)和 2,4-二硝基氯苯(DNCB)的小鼠 AD 模型来研究。此外,为了确定其作用的潜在机制,我们使用肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ)激活的角质形成细胞(HaCaT)。AEDKC 的口服给药可减少 AD 样皮肤损伤,表现为耳厚度、血清免疫球蛋白 E(IgE)、DFE 特异性 IgE、IgG2a、组胺水平和炎症细胞浸润减少。AEDKC 通过下调 HaCaT 细胞中的核因子-κB 和信号转导和转录激活因子 1,抑制促炎细胞因子和趋化因子的表达。在体内和体外检查 AD 相关因子时,证实 AEDKC 可减少 AD 样皮肤损伤。综上所述,结果表明 AEDKC 是治疗 AD 的潜在药物候选物。