首页> 外文期刊>Journal of biochemical and molecular toxicology >Local anesthetic articaine ameliorates LPS-induced acute kidney injury via inhibition of NF-κB activation and the NLRP3 inflammasome pathway
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Local anesthetic articaine ameliorates LPS-induced acute kidney injury via inhibition of NF-κB activation and the NLRP3 inflammasome pathway

机译:局部麻醉剂通过抑制NF-κB活化和NLRP3炎症途径来改善LPS诱导的急性肾损伤

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摘要

The present study was conducted to determine the protective effect of articaine (ART) in an lipopolysaccharide (LPS)-induced acute kidney injury (AKI) animal model. The results suggest ART causes a significant decrease in serum blood urea nitrogen, creatinine, and serum cystatin C level, showing a protective effect against LPS-induced AKI. This has been further supported by histopathological findings of kidney tissues. The level of tumor necrosis factor-α, interleukin (IL)-6, and IL-1β in serum and kidney tissues was remarkably inhibited by ART in a dose-dependent manner. ART causes a significant reduction of malondialdehyde and increases the activities of glutathione and superoxide dismutase with an increase in dose as compared to the LPS-treated group. Moreover, the ART-treated group showed dose-dependent inhibition of LPS-induced nuclear factor-κB activation and TLR4 expression as confirmed by Western blot analysis. The level of Bcl-2 family genes (Bcl-2 and Bax) was restored near to normal by ART. Collectively, all the above results indicated that ART had protective effects against LPS-induced AKI by blocking inflammatory and oxidative responses.
机译:本研究旨在确定阿替卡因(ART)在脂多糖(LPS)诱导的急性肾损伤(AKI)动物模型中的保护作用。结果表明,ART可显著降低血清尿素氮、肌酐和血清胱抑素C水平,对LPS诱导的AKI具有保护作用。肾脏组织的组织病理学结果进一步证实了这一点。ART可显著抑制血清和肾组织中肿瘤坏死因子-α、白细胞介素(IL)-6和IL-1β的水平,且呈剂量依赖性。与LPS治疗组相比,ART使丙二醛显著减少,并随着剂量的增加而增加谷胱甘肽和超氧化物歧化酶的活性。此外,经Western blot分析证实,ART治疗组对LPS诱导的核因子-κB激活和TLR4表达具有剂量依赖性抑制作用。通过ART,Bcl-2家族基因(Bcl-2和Bax)的水平恢复到接近正常水平。总之,上述所有结果表明ART通过阻断炎症和氧化反应对LPS诱导的AKI具有保护作用。

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