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荭草素通过抑制NF-κB通路和NLRP3炎性小体改善脂多糖诱导的炎症反应。

Orientin Ameliorates LPS-Induced Inflammatory Responses through the Inhibitory of the NF-B Pathway and NLRP3 Inflammasome.

作者信息

Xiao Qingfei, Qu Zhihui, Zhao Ying, Yang Liming, Gao Pujun

机构信息

Department of Hepatology, The First Hospital of Jilin University, Changchun 130021, China; Department of Nephrology, The First Hospital of Jilin University, Changchun 130021, China.

Department of Nephrology, The First Hospital of Jilin University, Changchun 130021, China.

出版信息

Evid Based Complement Alternat Med. 2017;2017:2495496. doi: 10.1155/2017/2495496. Epub 2017 Jan 19.

Abstract

Inflammation is a complex response to diverse pathological conditions, resulting in negative rather than protective effects when uncontrolled. Orientin (Ori), a flavonoid component isolated from natural plants, possesses abundant properties. Thus, we aimed to discover the potential therapeutic effects of orientin on lipopolysaccharide- (LPS-) induced inflammation in RAW 264.7 cells and the underlying mechanisms. In our studies, we evaluated the effects of Ori on proinflammatory mediator production stimulated by LPS, including tumor necrosis factor- (TNF-) , interleukin- (IL-) 6, IL-18, and IL-1, along with prostaglandin E (PGE) and NO. Our data indicated that orientin dramatically inhibited the levels of these mediators. Consistent with these results, the expression levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were also reduced. Further study demonstrated that such inhibitory effects of Ori were due to suppression of the nuclear factor-kappa B (NF-B) pathway and nucleotide-binding domain- (NOD-) like receptor protein 3 (NLRP3) inflammasome activation, which may contribute to its anti-inflammatory effects. Together, these findings show that Ori may be an effective candidate for ameliorating LPS-induced inflammatory responses.

摘要

炎症是对多种病理状况的复杂反应,若不受控制会产生负面而非保护作用。荭草素(Ori)是从天然植物中分离出的一种黄酮类成分,具有多种特性。因此,我们旨在探究荭草素对脂多糖(LPS)诱导的RAW 264.7细胞炎症的潜在治疗作用及其潜在机制。在我们的研究中,我们评估了荭草素对LPS刺激的促炎介质产生的影响,包括肿瘤坏死因子(TNF)、白细胞介素(IL)-6、IL-18和IL-1,以及前列腺素E(PGE)和一氧化氮(NO)。我们的数据表明,荭草素显著抑制了这些介质的水平。与这些结果一致,环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)的表达水平也降低了。进一步的研究表明,荭草素的这种抑制作用是由于抑制了核因子-κB(NF-κB)途径和核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎性小体的激活,这可能有助于其抗炎作用。总之,这些发现表明荭草素可能是改善LPS诱导的炎症反应的有效候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ca9/5288532/f104b9dde8db/ECAM2017-2495496.001.jpg

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