丙二醛
TLR4型
炎症体
超氧化物歧化酶
肌酐
药理学
脂多糖
血尿素氮
肾
急性肾损伤
氧化应激
肿瘤坏死因子α
胱抑素C
白细胞介素
医学
化学
炎症
内科学
细胞因子
作者
Guogang Zhao,Shan Lu,Linlin Li,Xiaodi Fan
摘要
Abstract 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.
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