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Anti‐inflammatory effects of rhaponticin on LPS‐induced human endothelial cells through inhibition of MAPK/NF‐κβ signaling pathways
Journal of Biochemical and Molecular Toxicology ( IF 3.6 ) Pub Date : 2021-02-18 , DOI: 10.1002/jbt.22733
Rougang Li 1 , Arunachalam Chinnathambi 2 , Sulaiman Ali Alharbi 2 , Omar H M Shair 2 , Vishnu Priya Veeraraghavan 3 , Krishna Mohan Surapaneni 4 , Thamaraiselvan Rengarajan 5
Affiliation  

The untreated systemic chronic inflammation leads to autoimmune diseases, hyperglycemia, cardiovascular diseases, type 2 diabetes, hypertension, osteoporosis, and so on. Phytochemicals effectively inhibit the inflammation, and numerous studies have proved that the phytocomponents possess anti‐inflammatory property via inhibiting the cyclooxygenase and lipoxygenase signaling pathways. Rhaponticin is one such phytochemical obtained from the perennial plant Rheum rhaponticum L. belonging to Polygonaceae family. We assessed the anti‐inflammatory potency of rhaponticin in endothelial cells induced with lipopolysaccharides (LPS). Four different endothelial cells induced with LPS were treated with rhaponticin and assessed for the nitric oxide generation. The cytotoxic potency of rhaponticin was evaluated in endothelial cells using the 3‐(4,5‐dimethylthizaol‐2yl)−2,5‐diphenyl tetrazolium bromide assay. The tumor necrosis factor‐α (TNF‐α) synthesis was quantified using the commercially available assay kit. The inflammatory signaling protein gene expression of TNF‐α, inducible nitric oxide synthase (iNOS), cyclooxygenase‐2 (COX2), and interleukin‐1β (IL‐1β) was analyzed with quantitative polymerase chain reaction (PCR) analysis. The gene expression of NADPH oxidase (NOX) cytoplasmic catalytic subunits gp91phox, p47phox, and p22phox was assessed with real‐time PCR analysis. Finally, to confirm the anti‐inflammatory potency of rhaponticin, the nuclear factor kappa B (NFκB) and mitogen‐activated protein kinase (MAPK) signaling protein expression was analyzed with immunoblotting analysis. Rhaponticin treatment significantly decreased the levels of nitric oxide and TNF‐α synthesis in LPS‐induced endothelial cells. It significantly decreased the gene expression of inflammatory proteins and NOX signaling protein. The protein expression of NFκB and MAPK signaling proteins was drastically decreased in rhaponticin‐treated endothelial cells induced with LPS. Overall, our results confirm that rhaponticin effectively inhibited the inflammation triggered by LPS in endothelial cells via downregulating iNOS, COX2, and NFκB and MAPK signaling pathways.

中文翻译:

rhaponticin通过抑制MAPK /NF-κβ信号通路对LPS诱导的人内皮细胞的抗炎作用

未经治疗的全身性慢性炎症会导致自身免疫性疾病,高血糖症,心血管疾病,2型糖尿病,高血压,骨质疏松症等。植物化学物质可有效抑制炎症,许多研究已证明植物成分可通过抑制环氧合酶和脂氧合酶的信号传导途径而具有抗炎特性。Rhaponticin是从多年生植物大黄(Rheum rhaponticum)中获得的一种植物化学物质。属于Poly科的L.。我们评估了脂多糖(LPS)诱导的内皮素在内皮细胞中的抗炎作用。用鼠李糖苷处理用LPS诱导的四种不同的内皮细胞,并评估一氧化氮的产生。使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四氮唑测定法评估了内皮素在鼠肝素中的细胞毒性。肿瘤坏死因子-α(TNF-α)的合成使用市售的测定试剂盒进行定量。使用定量聚合酶链反应(PCR)分析了TNF-α,诱导型一氧化氮合酶(iNOS),环氧合酶-2(COX2)和白介素-1β(IL-1β)的炎症信号蛋白基因表达。NADPH氧化酶(NOX)细胞质催化亚基gp91的基因表达phox,p47 phox和p22 phox通过实时PCR分析进行评估。最后,为了确定鼠李糖苷的抗炎能力,使用免疫印迹分析法分析了核因子κB(NFκB)和有丝分裂原激活的蛋白激酶(MAPK)信号蛋白的表达。Rhaponticin处理可显着降低LPS诱导的内皮细胞中一氧化氮和TNF-α的合成水平。它显着降低了炎症蛋白和NOX信号蛋白的基因表达。在LPS诱导的鼠藤黄素处理的内皮细胞中,NFκB和MAPK信号传导蛋白的蛋白表达急剧下降。总体而言,我们的结果证实,Rhapponticin可通过下调iNOS,COX2,NFκB和MAPK信号通路有效抑制内皮细胞中LPS触发的炎症。
更新日期:2021-02-18
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