首页> 外文期刊>European Journal of Pharmacology: An International Journal >Tenuigenin exhibits protective effects against LPS-induced acute kidney injury via inhibiting TLR4/NF-kappa B signaling pathway
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Tenuigenin exhibits protective effects against LPS-induced acute kidney injury via inhibiting TLR4/NF-kappa B signaling pathway

机译:Tenuigenin通过抑制TLR4 /NF-κB信号通路对LPS诱导的急性肾脏损伤具有保护作用

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Tenuigenin (TNG) has been reported to have various pharmacological activities, such as anti-oxidative and anti-inflammatory activities. However, the protective effects of TNG on lipopolysaccharides (LPS)induced acute kidney injury (AKI) are still not clear. The aim of this study was to investigate the protective effects and mechanism of TGN on LPS-induced AKI in mice. The kidney histological change, levels of blood urea nitrogen (BUN), and creatinine were measured to assess the protective effects of TNG on LPS-induced AKI. The levels of TNIF-alpha, IL-1 beta, and IL-6 in serum and kidney tissues were detected by ELISA. The extent of nuclear factor kappa-B (NF-kappa B) p65 and the expression of Toll-like receptor-4 (TLR4) were detected by western blot analysis. The results showed that TNG markedly attenuated the histological alterations, BUN and creatinine levels in kidney. TNG also suppressed LPS-induced TNIF-alpha, IL-1 beta, and IL-6 production. Furthermore, the expression of TLR4 and NF-kappa B activation induced by LPS were markedly inhibited by TNG. In conclusion, this study demonstrated that TNG protected against LPS-induced AKI by inhibiting TLR4/NF-kappa B signaling pathway. (C) 2016 Elsevier B.V. All rights reserved.
机译:Tenuigenin(TNG)已报道具有多种药理活性,例如抗氧化和抗炎活性。但是,TNG对脂多糖(LPS)诱导的急性肾损伤(AKI)的保护作用仍不清楚。这项研究的目的是研究TGN对LPS诱导的小鼠AKI的保护作用和机制。测量肾脏的组织学变化,血尿素氮(BUN)和肌酐水平,以评估TNG对LPS诱导的AKI的保护作用。通过ELISA检测血清和肾脏组织中TNIF-α,IL-1β和IL-6的水平。通过蛋白质印迹分析检测核因子κB(NF-κB)p65的程度和Toll样受体4(TLR4)的表达。结果表明,TNG明显减轻了肾脏的组织学改变,BUN和肌酐水平。 TNG还抑制LPS诱导的TNIF-alpha,IL-1 beta和IL-6的产生。此外,由TNG明显抑制LPS诱导的TLR4的表达和NF-κB的活化。总之,这项研究表明,TNG通过抑制TLR4 /NF-κB信号通路来保护LPS诱导的AKI。 (C)2016 Elsevier B.V.保留所有权利。

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