Orientin Ameliorates LPS-Induced Inflammatory Responses through the Inhibitory of the NF-κB Pathway and NLRP3 Inflammasome.
作者： Qingfei Xiao , Zhihui Qu , Ying Zhao , Liming Yang , Pujun Gao
DOI: 10.1155/2017/2495496
关键词: Pharmacology 、 NF-κB 、 Immunology 、 Biology 、 Lipopolysaccharide 、 Tumor necrosis factor alpha 、 Nitric oxide synthase 、 Inflammation 、 Orientin 、 Inflammasome 、 Proinflammatory cytokine
摘要: Inflammation is a complex response to diverse pathological conditions, resulting in negative rather than protective effects when uncontrolled. Orientin (Ori), flavonoid component isolated from natural plants, possesses abundant properties. Thus, we aimed discover the potential therapeutic of orientin on lipopolysaccharide- (LPS-) induced inflammation RAW 264.7 cells and underlying mechanisms. In our studies, evaluated Ori proinflammatory mediator production stimulated by LPS, including tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, IL-18, IL-1β, along with prostaglandin E2 (PGE2) NO. Our data indicated that dramatically inhibited levels these mediators. Consistent results, expression cyclooxygenase-2 (COX-2) inducible nitric oxide synthase (iNOS) were also reduced. Further study demonstrated such inhibitory due suppression nuclear factor-kappa B (NF-κB) pathway nucleotide-binding domain- (NOD-) like receptor protein 3 (NLRP3) inflammasome activation, which may contribute its anti-inflammatory effects. Together, findings show be an effective candidate for ameliorating LPS-induced inflammatory responses.
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Yiren Wang, Yuting Cui, Fayang Cao, Yiyang Qin, Wenjing Li, Jinghai Zhang, Ganglioside GD1a suppresses LPS-induced pro-inflammatory cytokines in RAW264.7 macrophages by reducing MAPKs and NF-κB signaling pathways through TLR4 International Immunopharmacology. ,vol. 28, pp. 136- 145 ,(2015) , 10.1016/J.INTIMP.2015.05.044
B. Brooks-Worrell, J. P. Palmer, Immunology in the Clinic Review Series; focus on metabolic diseases: development of islet autoimmune disease in type 2 diabetes patients: potential sequelae of chronic inflammation. Clinical and Experimental Immunology. ,vol. 167, pp. 40- 46 ,(2012) , 10.1111/J.1365-2249.2011.04501.X
Sergei S Makarov, NF-κB in rheumatoid arthritis: a pivotal regulator of inflammation, hyperplasia, and tissue destruction Arthritis Research & Therapy. ,vol. 3, pp. 200- 206 ,(2001) , 10.1186/AR300
Fabio Martinon, Kimberly Burns, Jürg Tschopp, The Inflammasome Molecular Cell. ,vol. 10, pp. 417- 426 ,(2002) , 10.1016/S1097-2765(02)00599-3
Tucker Collins, Myron I. Cybulsky, NF-κB: pivotal mediator or innocent bystander in atherogenesis? Journal of Clinical Investigation. ,vol. 107, pp. 255- 264 ,(2001) , 10.1172/JCI10373
Lida A. Beninson, Monika Fleshner, Exosomes in fetal bovine serum dampen primary macrophage IL-1β response to lipopolysaccharide (LPS) challenge Immunology Letters. ,vol. 163, pp. 187- 192 ,(2015) , 10.1016/J.IMLET.2014.10.019
Michael D. Schwartz, Ernest E. Moore, Frederick A. Moore, Robert Shenkar, Pierre Moine, James B. Haenel, Edward Abraham, Nuclear factor-kappa B is activated in alveolar macrophages from patients with acute respiratory distress syndrome. Critical Care Medicine. ,vol. 24, pp. 1285- 1292 ,(1996) , 10.1097/00003246-199608000-00004
Osamu Takeuchi, Hideki Sanjo, Katsuaki Hoshino, Yoshifumi Takeda, Kiyoshi Takeda, Shizuo Akira, Tomohiko Ogawa, Taro Kawai, Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. Journal of Immunology. ,vol. 162, pp. 3749- 3752 ,(1999)
Luigi Franchi, Tatjana Eigenbrod, Raúl Muñoz-Planillo, Gabriel Nuñez, The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis. Nature Immunology. ,vol. 10, pp. 241- 247 ,(2009) , 10.1038/NI.1703
Li Cui, Liang Feng, Zhen Hai Zhang, Xiao Bin Jia, The anti-inflammation effect of baicalin on experimental colitis through inhibiting TLR4/NF-κB pathway activation. International Immunopharmacology. ,vol. 23, pp. 294- 303 ,(2014) , 10.1016/J.INTIMP.2014.09.005