Dexmedetomidine Alleviates Acute Stress-Induced Acute Kidney Injury by Attenuating Inflammation and Oxidative Stress via Inhibiting the P2X7R/NF-κB/NLRP3 Pathway in Rats

文献类型： 外文期刊

第一作者： Yang, Haotian

作者： Yang, Haotian;Zhao, Yuan;Yang, Tianyuan;Dou, Xinyi;Li, Junfeng;Feng, Guofeng;Fan, Honggang;Zhang, Shuai;Yang, Haotian;Chen, Yongping;Yang, Guiyan;Fang, Hao

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关键词： dexmedetomidine; acute stress; kidney; oxidative stress; inflammation; P2X(7)R/NF-kappa B/NLRP3

期刊名称：INFLAMMATION （ 影响因子：4.5； 五年影响因子：4.6 ）

ISSN： 0360-3997

年卷期： 2024 年

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收录情况： SCI

摘要： This study aimed to investigate the potential protective effects of Dexmedetomidine (DEX) against acute kidney injury (AKI) induced by acute stress (AS). Wistar rats were divided into five groups: Control, DEX, AS, AS + DEX, and AS + A438079. The results showed that AS led to AKI by increasing inflammatory biomarkers and oxidative stress-related indicators. The acute stress model in rats was successfully established. Renal function, histopathology, oxidative stress, and inflammation were assessed. Localization of P2X7 receptor (P2X7R) was determined by immunofluorescence. Additionally, the key inflammatory proteins of the P2X7R/NF-kappa B/NLRP3 signaling pathway were measured by Western blotting. DEX significantly improved kidney function, alleviated kidney injury, and reduced oxidative stress and inflammation. DEX inhibited the activation of the P2X7R, decreased the expression of NF-kappa B, NLRP3 inflammasome, and Caspase-1, and inhibited the expression of interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). Furthermore, DEX also alleviated AS-induced AKI by inhibiting the excessive production of reactive oxygen species (ROS) and reducing oxidative stress. In conclusion, DEX attenuates AS-induced AKI by mitigating inflammation and oxidative stress through the inhibition of the P2X7R/NF-kappa B/NLRP3 pathway in rats.

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