Zhao Guanjie, Lu Shan, Li Linlin, Fan Xiaodi
Department of Nephrology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Department of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
J Biochem Mol Toxicol. 2020 Oct;34(10):e22554. doi: 10.1002/jbt.22554. Epub 2020 Jul 20.
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.
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可使血清血尿素氮、肌酐和血清胱抑素C水平显著降低，显示出对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支持了这一点。ART以剂量依赖性方式显著抑制血清和肾脏组织中肿瘤坏死因子-α、白细胞介素（IL）-6和IL-1β的水平。与LPS处理组相比，ART可显著降低丙二醛水平，并随着剂量增加提高谷胱甘肽和超氧化物歧化酶的活性。此外，蛋白质免疫印迹分析证实，ART处理组对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。ART使Bcl-2家族基因（Bcl-2和Bax）水平恢复至接近正常。综上所述，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。
