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山柰在角质形成细胞和巨噬细胞中的抗银屑病和抗炎作用。

Anti-psoriatic and anti-inflammatory effects of Kaempferia parviflora in keratinocytes and macrophage cells.

机构信息

Department of Pharmacology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Research Center of Pharmaceutical Nanotechnology, Faculty of Pharmacy, Chiang Mai University, Chiang Mai, Thailand.

Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

出版信息

Biomed Pharmacother. 2021 Nov;143:112229. doi: 10.1016/j.biopha.2021.112229. Epub 2021 Sep 24.

Abstract

Kaempferia parviflora (KP) has been used as folk medicine for curing various conditions, including anti-inflammatory diseases. However, anti-psoriatic effects in an aspect of suppression of NF-κB activation have not been explored. Therefore, our current study aimed to elucidate the anti-inflammation of KP in lipopolysaccharide (LPS)-induced RAW264.7 cells and anti-psoriatic effects of KP in cytokine-induced human keratinocytes, HaCaT cells. We discovered that KP extract significantly suppressed LPS-induced inflammation at both gene expression and protein production. Specifically, dramatic reduction of nitric oxide (NO) was explored by using Griess method. Consistently, data from RT-qPCR, ELISA, and western blot analysis confirmed that crucial inflammatory and psoriatic markers including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, IL-17, IL-22, and IL-23 were significantly decreased by the action of KP. These events were associated with the results from immunofluorescence study and western blot analysis where the activation of NF-κB upon LPS stimulation was clearly inhibited by KP through its ability to suppress IκB-α degradation resulting in inhibition of NF-κB nuclear translocation. Furthermore, KP extract significantly inhibited LPS-stimulated phosphorylation of ERK1/2, JNK, and p38 in a dose-dependent manner, along with inhibition of ERK1/2 activation in both TNF-α- and EGF-induced HaCaT cells. Interestingly, HaCaT cells exposed to 15 μg/mL of KP also exhibited significant decrease of cell migration and proliferation. Our results revealed that KP extract has a potential to be developed as a promising agent for treating inflammation and psoriasis, in part through targeting the proliferation and the NF-κB pathways.

摘要

山柰(KP)已被用作治疗各种疾病的民间药物,包括抗炎疾病。然而,在抑制 NF-κB 激活方面的抗银屑病作用尚未得到探索。因此,我们目前的研究旨在阐明 KP 在脂多糖(LPS)诱导的 RAW264.7 细胞中的抗炎作用和 KP 在细胞因子诱导的人角质形成细胞(HaCaT 细胞)中的抗银屑病作用。我们发现 KP 提取物可显著抑制 LPS 诱导的炎症,无论是在基因表达还是蛋白质产生方面。具体而言,通过使用 Griess 法探讨了一氧化氮(NO)的急剧减少。一致地,RT-qPCR、ELISA 和 Western blot 分析的数据证实了关键的炎症和银屑病标志物,包括诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1、IL-6、IL-17、IL-22 和 IL-23 均显著减少。这些事件与免疫荧光研究和 Western blot 分析的结果相关,其中 KP 通过抑制 IκB-α 降解从而抑制 NF-κB 核易位,明显抑制 LPS 刺激引起的 NF-κB 激活。此外,KP 提取物以剂量依赖性方式显著抑制 LPS 刺激的 ERK1/2、JNK 和 p38 的磷酸化,同时抑制 TNF-α和 EGF 诱导的 HaCaT 细胞中 ERK1/2 的激活。有趣的是,暴露于 15μg/mL KP 的 HaCaT 细胞也表现出细胞迁移和增殖的显著减少。我们的结果表明,KP 提取物具有开发为治疗炎症和银屑病的有前途药物的潜力,部分通过针对增殖和 NF-κB 途径。

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