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首页> 外文期刊>Inflammopharmacology >Jungia sellowii suppresses the carrageenan-induced inflammatory response in the mouse model of pleurisy.
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Jungia sellowii suppresses the carrageenan-induced inflammatory response in the mouse model of pleurisy.

机译:Jungia sellowii在胸膜炎小鼠模型中抑制了角叉菜胶诱导的炎症反应。

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摘要

This study was conducted to explore the anti-inflammatory effect of Jungia sellowii (Asteraceae) using a murine model of pleurisy induced by carrageenan (Cg). This plant is used in southern Brazil to treat inflammatory diseases. J. sellowii leaves were extracted with ethanol/water to obtain the crude extract (CE), which was fractionated with different solvents, yielding n-hexane (Hex), dichloromethane (DCM), ethyl acetate (EtOAc) and n-butanol (BuOH) fractions, and aqueous fraction (Aq). The major compounds succinic acid (SA) and lactic acid (LA) were isolated from Aq fraction, and their structures were determined by (1)H and (13)C NMR. Pleurisy was induced by Cg (Saleh et al. 1996). The leukocytes, exudation, myeloperoxidase (MPO) and adenosine-deaminase (ADA) activities, metabolites of nitric oxide (NO x ) levels, protein levels and mRNA expression for interleukin 1 beta (IL-1β), tumour necrosis factor alpha (TNF-α), interleukin 17A (IL17A) and inducible of nitric oxide synthase (iNOs), and p65 protein phosphorylation (NF-κB) were analysed 4?h after pleurisy induction. Animals pre-treated with CE, BuOH, Aq, SA, or LA inhibited leukocytes, exudation, MPO and ADA activities, NO x , IL-1β, TNF-α, and IL-17A levels, and the mRNA expression for IL-1β, TNF-α, IL-17A, iNOS, and p65 protein phosphorylation (NF-κB) (p?
机译:这项研究进行了探讨使用角叉菜胶(Cg)诱导的胸膜炎的小鼠模型对Jungung sellowii(菊科)的抗炎作用。该植物在巴西南部用于治疗炎症。用乙醇/水提取J. sellowii叶,得到粗提取物(CE),将其用不同的溶剂分馏,得到正己烷(Hex),二氯甲烷(DCM),乙酸乙酯(EtOAc)和正丁醇(BuOH) )馏分和水相馏分(Aq)。从Aq级分中分离出主要化合物琥珀酸(SA)和乳酸(LA),并通过(1)H和(13)C NMR确定其结构。胸膜炎是由Cg引起的(Saleh等,1996)。白细胞,渗出液,髓过氧化物酶(MPO)和腺苷脱氨酶(ADA)活性,一氧化氮(NO x)水平的代谢产物,白细胞介素1 beta(IL-1β)的蛋白质水平和mRNA表达,肿瘤坏死因子α(TNF-胸膜炎诱导后4?h对白细胞介素17A(IL17A)和一氧化氮合酶(iNOs)的诱导物和p65蛋白磷酸化(NF-κB)进行了分析。用CE,BuOH,Aq,SA或LA预处理的动物抑制白细胞,渗出,MPO和ADA活性,NO x,IL-1β,TNF-α和IL-17A水平以及IL-1β的mRNA表达,TNF-α,IL-17A,iNOS和p65蛋白磷酸化(NF-κB)(p 0.05)。我们的研究表明,J。Sellowii可以通过减少白细胞和渗出而防止Cg引起的炎症。其作用与促炎细胞因子和/或NO x的减少有关。通过抑制所有研究参数,分离出的化合物SA和LA可能在这种抗炎作用中发挥重要作用。这些化合物的抗炎特性归因于NF-κB的下调。

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