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Paeoniflorin protects against concanavalin A-induced hepatitis in mice

机译:eon药苷可预防伴刀豆球蛋白A引起的小鼠肝炎

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摘要

Paeoniflorin (PF) is one of the main effective components of the total glucosides of peony, which has been reported to have anti-inflammatory ability. However, the effects of paeoniflorin on concanavalin A (Con A)-induced hepatitis have not been carefully examined. The aim of this study was to investigate the protective effect of paeoniflorin and elucidate potential mechanisms of paeoniflorin on Con A-induced hepatitis. C57BL/6 mice were divided randomly into the following four experimental groups: PBS group, PF group, Con A group, and Con A + PF group. Mice received paeoniflorin (50 mg/kg) by tail vein before Con A intravenous administration. We found that paeoniflorin pretreatment can significantly reduce the elevated plasma aminotransferase levels and liver necrosis in Con A-induced hepatitis. Also, paeoniflorin pretreatment suppressed the secretion of proinflainmatory cytokines (TNF-alpha, INF-gamma, IL-6), compared with Con A group. Meanwhile, paeoniflorin pretreatment decreased CD4(+), CD8(+) and NKT cell infiltration in the liver. Besides, we observed that paeoniflorin pretreatment can decrease the expression level of Toll-like receptor CUR) 4 mRNA or protein in liver tissues. Further results showed that paeoniflorin pretreatment was capable of suppressing the activation of the NF-kappa B pathway by inhibiting I kappa B alpha kinase and p65 phosphorylation in Con A-induced liver injury. These results suggest that paeoniflorin pretreatment protects mice against Con A-induced liver injury via inhibition of several inflammatory mediators and, at least in part, by suppressing CD4(+), CD8(+) and NKT cell infiltration in liver. The beneficial effect of paeoniflorin may be related to the downregulation of TLR4 expression and the inhibition of NF-kappa B activation. (C) 2014 Elsevier B.V. All rights reserved.
机译:eon药苷(PF)是牡丹总苷的主要有效成分之一,据报道具有抗炎能力。但是,pa药苷对伴刀豆球蛋白A(Con A)诱导的肝炎的作用尚未得到仔细检查。这项研究的目的是调查of药苷的保护作用,并阐明of药苷对Con A诱导的肝炎的潜在作用机制。将C57BL / 6小鼠随机分为以下四个实验组:PBS组,PF组,Con A组和Con A + PF组。在Con A静脉内给药之前,小鼠通过尾静脉接受pa药苷(50 mg / kg)。我们发现pa药苷预处理可以显着降低Con A诱导的肝炎患者血浆转氨酶水平升高和肝坏死。此外,与Con A组相比,pa药花青素预处理可抑制前炎症细胞因子(TNF-α,INF-γ,IL-6)的分泌。同时,pa药苷预处理可降低肝脏中CD4(+),CD8(+)和NKT细胞的浸润。此外,我们观察到pa药苷预处理可降低肝脏组织中Toll样受体CUR)4 mRNA或蛋白的表达水平。进一步的结果表明,pa药苷预处理能够通过抑制Con A诱导的肝损伤中的IκBα激酶和p65磷酸化来抑制NF-κB通路的激活。这些结果表明pa药苷预处理可通过抑制几种炎症介质并至少部分通过抑制肝脏中的CD4(+),CD8(+)和NKT细胞浸润来保护小鼠免受Con A诱导的肝损伤。 eon药苷的有益作用可能与下调TLR4表达和抑制NF-κB活化有关。 (C)2014 Elsevier B.V.保留所有权利。

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