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