首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Farrerol Relieve Lipopolysaccharide (LPS)-Induced Mastitis by Inhibiting AKT/NF-κB p65 ERK1/2 and P38 Signaling Pathway
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Farrerol Relieve Lipopolysaccharide (LPS)-Induced Mastitis by Inhibiting AKT/NF-κB p65 ERK1/2 and P38 Signaling Pathway

机译:Farrerol通过抑制AKT /NF-κBp65ERK1 / 2和P38信号通路缓解脂多糖(LPS)诱导的乳腺炎

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摘要

Farrerol has been proved to have an anti-inflammatory effect. However, the effects of farrerol on mastitis have not been investigated. This study was aimed to investigate the effect and mechanism of farrerol in lipopolysaccharide (LPS)-induced mouse mastitis and LPS-induced inflammatory response of mouse mammary epithelial cells (mMECs). In vivo, LPS were injected to the tetrad pair of nipples for establishing mouse mastitis, and then tested the effect of farrerol on histopathological changes, inflammatory response and activation degree of protein kinase B (AKT), nuclear factor-kappa B p65 (NF-κB p65), p38, extracellular regulated protein kinase (ERK1/2). In vitro, the mMECs were incubated by farrerol for 1 h following by stimulating with LPS, and then the inflammatory response and the related signaling pathways were detected. The in vivo results found that farrerol could improve pathological injury of mammary gland, attenuate the activity of myeloperoxidase (MPO), inhibit the production of pro-inflammatory mediators and the phosphorylation of AKT, NF-κB p65, p38 and ERK1/2. The in vitro results also found farrerol inhibited inflammatory response and the related signaling pathways. Collectively, this study revealed that farrerol inhibits the further development of LPS-induced mastitis by inhibiting inflammatory response via down regulating phosphorylation of AKT, NF-κB p65, p38, and ERK1/2. These findings suggest that farrerol may be used as an anti-inflammatory drug for mastitis.
机译:法雷洛尔已被证明具有抗炎作用。然而,尚未研究法瑞洛对乳腺炎的作用。本研究旨在探讨法瑞罗在脂多糖(LPS)诱导的小鼠乳腺炎和LPS诱导的小鼠乳腺上皮细胞(mMECs)的炎症反应中的作用和机制。在体内,将LPS注射到四对乳头中以建立小鼠乳腺炎,然后测试法瑞洛尔对组织病理学变化,炎症反应和蛋白激酶B(AKT),核因子-κBp65(NF- κBp65),p38,细胞外调节蛋白激酶(ERK1 / 2)。在体外,通过用LPS刺激将mMEC通过法瑞罗尔孵育1小时,然后检测炎症反应和相关的信号传导途径。体内结果表明,法雷洛尔可以改善乳腺的病理损伤,减弱髓过氧化物酶(MPO)的活性,抑制促炎性介质的产生以及AKT,NF-κBp65,p38和ERK1 / 2的磷酸化。体外结果还发现,法雷洛尔抑制炎症反应和相关的信号通路。总体而言,这项研究表明,法雷洛尔通过下调AKT,NF-κBp65,p38和ERK1 / 2的磷酸化来抑制炎症反应,从而抑制LPS诱发的乳腺炎的进一步发展。这些发现表明,法瑞罗可以用作乳腺炎的消炎药。

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