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提取物通过调节 BALB/c 小鼠的 MAPK 信号通路来减轻特应性皮炎样皮肤损伤。

Extract Attenuates Atopic Dermatitis-Like Skin Lesions through Modulation of MAPK Signaling in BALB/c Mice.

机构信息

Department of Pharmacy, College of Pharmacy, Dankook University, Dandae-ro 119, Dongnam, Cheonan, Chungnam 31116, Korea.

Bio-Center, Gyeonggido Business and Science Accelerator, Gwanggyo-ro 147, Yeoungtong, Suwon, Gyeonggi 16229, Korea.

出版信息

Molecules. 2020 Apr 24;25(8):2003. doi: 10.3390/molecules25082003.

Abstract

Atopic dermatitis (AD) is a chronic inflammatory disease. () is used as a traditional medicine to improve various pathologies in Southeast Asia. In this study, we investigated the effects of ethanol extract (CQ) on 1-chloro-2,4-dinitrobenzene (DNCB)-induced AD like skin lesions in BALB/c mice. After administration with CQ (100, 200, and 400 mg/kg) for 6 weeks, AD symptoms, protein expression, immunoglobulin E (IgE), thymus and activation-regulated chemokine (TARC), and ceramidase level were measured in skin lesions of DNCB-induced BALB/c mice. CQ group improved the dermatitis score, skin pH, transepidermal water loss (TEWL), and skin hydration. Furthermore, histological analysis revealed that CQ attenuated the increased epidermal thickness and infiltration of mast cells caused by DNCB. CQ also increased the expression of filaggrin, and reduced the expression of ceramidase, serum IgE level, and the number of eosinophils. CQ effectively inhibited cytokines and chemokines such as interleukin (IL)-6, IL-13, TARC, and thymic stromal lymphopoietin (TSLP) at the mRNA levels, as well as the activation of mitogen-activated protein kinase (MAPK), including extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 in the skin lesions. Taken together, these findings demonstrate that CQ may be an effective treatment of AD-like skin lesions by inhibiting the expression of inflammatory mediators via the MAPK signaling pathways.

摘要

特应性皮炎(AD)是一种慢性炎症性疾病。(它)被用作传统药物,用于改善东南亚的各种病理状况。在这项研究中,我们研究了乙醇提取物(CQ)对 BALB/c 小鼠 1-氯-2,4-二硝基苯(DNCB)诱导的 AD 样皮肤损伤的影响。在给予 CQ(100、200 和 400mg/kg)6 周后,测量 DNCB 诱导的 BALB/c 小鼠皮肤损伤中的 AD 症状、蛋白质表达、免疫球蛋白 E(IgE)、胸腺激活调节趋化因子(TARC)和神经酰胺酶水平。CQ 组改善了皮炎评分、皮肤 pH 值、经表皮水分流失(TEWL)和皮肤水分。此外,组织学分析显示 CQ 减轻了 DNCB 引起的表皮厚度增加和肥大细胞浸润。CQ 还增加了丝聚蛋白的表达,降低了神经酰胺酶、血清 IgE 水平和嗜酸性粒细胞的数量。CQ 有效抑制了细胞因子和趋化因子,如白细胞介素(IL)-6、IL-13、TARC 和胸腺基质淋巴细胞生成素(TSLP),在 mRNA 水平,以及丝裂原激活蛋白激酶(MAPK)的激活,包括细胞外信号调节激酶(ERK)、c-jun N-末端激酶(JNK)和皮肤损伤中的 p38。总之,这些发现表明 CQ 可能通过抑制 MAPK 信号通路中炎症介质的表达,成为治疗 AD 样皮肤损伤的有效药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df59/7221768/021e1a00e009/molecules-25-02003-g0A1.jpg

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