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(皮埃尔)丹迪提取物通过调节小鼠巨噬细胞RAW 264.7细胞中的NF-κB信号通路和p38来抑制脂多糖诱导的诱导型一氧化氮合酶和一氧化氮

(Pierre) Dandy Extract Suppresses LPS-Induced iNOS and NO via Regulation of NF-κB Pathways and p38 in Murin Macrophage RAW 264.7 Cells.

作者信息

So Bo Ram, Bach Tran The, Paik Jin Hyub, Jung Sung Keun

机构信息

School of Food Science and Biotechnology, Kyungpook National University, Daegu 41566, Korea.

Institute of Ecology and Biological Resources, Vietnam Academy of Science and Technology (VAST), Ha Noi 100000, Vietnam.

出版信息

Prev Nutr Food Sci. 2020 Jun 30;25(2):166-172. doi: 10.3746/pnf.2020.25.2.166.

DOI:10.3746/pnf.2020.25.2.166
PMID:32676468
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7333012/
Abstract

Development of anti-inflammatory products remains in high demand due to the incidence of inflammatory diseases, including diabetes, cardiovascular disease, and neurodegenerative diseases. In this study, we examined the potential anti-inflammatory activity of the nutraceutical, (Pierre) Dandy extract (KDE). We evaluated the ability of KDE to inhibit lipopolysaccharide (LPS)-induced inflammatory markers, including nitric oxide (NO), nuclear factor kappa-B, and mitogen-activated protein kinases, in RAW 264.7 cells. KDE suppressed LPS-induced nitrite production and inducible NO synthase (iNOS) expression in RAW 264.7 cells, but has no effect on cyclooxygenase-2 expression. KDE also suppressed LPS-induced phosphorylation of p65, IκB kinase, and p38 in RAW 264.7 cells. Through Western blot assays and immunofluorescence results, we showed that KDE suppresses LPS-induced p65 translocation from cytosol to the nucleus in RAW 264.7 cells. Moreover, KDE suppressed mRNA expression of LPS-induced interleukin (IL)-1β in RAW 264.7 cells, but had no effect on mRNA expression of IL-6 or tumor necrosis factor-a. These results demonstrate that KDE may be a promising anti-inflammatory nutraceutical. KDE may act by suppressing iNOS expression and subsequent NO production by inhibiting phosphorylation of p65 and p38 and suppressing translocation of p65 from the cytosol to the nucleus.

摘要

由于包括糖尿病、心血管疾病和神经退行性疾病在内的炎症性疾病的发病率,抗炎产品的开发需求仍然很高。在本研究中,我们检测了营养保健品皮埃尔山龙眼提取物(KDE)的潜在抗炎活性。我们评估了KDE抑制脂多糖(LPS)诱导的RAW 264.7细胞中炎症标志物的能力,这些标志物包括一氧化氮(NO)、核因子κB和丝裂原活化蛋白激酶(MAPK)。KDE抑制RAW 264.7细胞中LPS诱导的亚硝酸盐产生和诱导型一氧化氮合酶(iNOS)表达,但对环氧合酶-2表达没有影响。KDE还抑制RAW 264.7细胞中LPS诱导的p65、IκB激酶和p38的磷酸化。通过蛋白质免疫印迹分析和免疫荧光结果,我们表明KDE抑制RAW 264.7细胞中LPS诱导的p65从细胞质向细胞核的转位。此外,KDE抑制RAW 264.7细胞中LPS诱导的白细胞介素(IL)-1β 的mRNA表达,但对IL-6或肿瘤坏死因子-α 的mRNA表达没有影响。这些结果表明,KDE可能是一种有前景的抗炎营养保健品。KDE可能通过抑制iNOS表达以及随后的NO产生来发挥作用,其机制可能是通过抑制p65和p38的磷酸化以及抑制p65从细胞质向细胞核的转位。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/be4890fdc7c5/PNFS-25-166-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/049d2008b57a/PNFS-25-166-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/658aba8513e9/PNFS-25-166-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/92c3ff07fc83/PNFS-25-166-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/9761c5b3390d/PNFS-25-166-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/be4890fdc7c5/PNFS-25-166-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/049d2008b57a/PNFS-25-166-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/658aba8513e9/PNFS-25-166-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/92c3ff07fc83/PNFS-25-166-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/9761c5b3390d/PNFS-25-166-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d84/7333012/be4890fdc7c5/PNFS-25-166-f5.jpg

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