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哈普洛平可改善2,4-二硝基氯苯诱导的小鼠特应性皮炎样皮肤损伤以及肿瘤坏死因子-α/干扰素-γ诱导的人角质形成细胞炎症。

Haplopine Ameliorates 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis-Like Skin Lesions in Mice and TNF-α/IFN-γ-Induced Inflammation in Human Keratinocyte.

作者信息

Kim Tae-Young, Kim Ye Jin, Jegal Jonghwan, Jo Beom-Geun, Choi Han-Seok, Yang Min Hye

机构信息

College of Pharmacy, Pusan National University, Busan 46241, Korea.

C&D Research Team, R&D Strategy Center, Genuonesciences, Seoul 06800, Korea.

出版信息

Antioxidants (Basel). 2021 May 19;10(5):806. doi: 10.3390/antiox10050806.

Abstract

This study aimed to investigate the anti-inflammatory, antioxidant, and anti-atopic dermatitis (AD) effects of haplopine, which is one of the active components in Haplopine (12.5 and 25 μM) inhibited the mRNA expressions of inflammatory cytokines IL-6, TSLP, GM-CSF, and G-CSF and the protein expressions of IL-6 and GM-CSF in TNF-α/INF-γ-stimulated HaCaT cells. In HO-induced Jukat T cells, haplopine (25 and 50 μM) suppressed the productions of proinflammatory cytokines (IL-4, IL-13, and COX-2) and increased the mRNA and protein expressions of oxidative stress defense enzymes (SOD, CAT, and HO-1) in a concentration-dependent manner. In vivo, haplopine significantly attenuated the development of AD symptoms in 2,4-dinitrochlorobenzene (DNCB)-stimulated Balb/c mice, as evidenced by reduced clinical dermatitis scores, skin thickness measurements, mast cell infiltration, and serum IgE concentrations. These findings demonstrate that haplopine should be considered a novel anti-atopic agent with the potential to treat AD.

摘要

本研究旨在探讨哈普洛平的抗炎、抗氧化和抗特应性皮炎(AD)作用,哈普洛平是裂叶荆芥中的活性成分之一。哈普洛平(12.5和25 μM)抑制了TNF-α/INF-γ刺激的HaCaT细胞中炎性细胞因子IL-6、TSLP、GM-CSF和G-CSF的mRNA表达以及IL-6和GM-CSF的蛋白表达。在HO诱导的Jukat T细胞中,哈普洛平(25和50 μM)以浓度依赖的方式抑制促炎细胞因子(IL-4、IL-13和COX-2)的产生,并增加氧化应激防御酶(SOD、CAT和HO-1)的mRNA和蛋白表达。在体内,哈普洛平显著减轻了2,4-二硝基氯苯(DNCB)刺激的Balb/c小鼠AD症状的发展,临床皮炎评分降低、皮肤厚度测量值减小、肥大细胞浸润减少以及血清IgE浓度降低均证明了这一点。这些发现表明,哈普洛平应被视为一种具有治疗AD潜力的新型抗特应性药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9fa/8161082/b8a5e149a541/antioxidants-10-00806-g001.jpg

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