右美托咪定抑制NOX4缓解急性应激致大鼠肾损伤

本研究拟探索右美托咪定（dexmedetomidine，DEX）对大鼠急性应激致肾损伤的保护作用，并从氧化应激的角度探索DEX对大鼠肾的保护通路。本研究使用了急性束缚应激模型，其中，大鼠被迫游泳15 min，并束缚3 h。本试验采用生化检测、组织病理学切片观察以评估肾功能，然后测定了氧化应激以及氧化应激的相关通路蛋白。旷场试验证实成功建立了急性应激模型。急性应激引起的肾损伤增加了NOX4，降低了Nrf2/HO-1/NQO1表达水平。DEX可降低NOX4表达，同时升高Nrf2/HO-1/NQO1的表达水平。DEX治疗组与急性应激组相比的肾生化结果明显恢复正常，病理切片观察损伤显著降低。试验结果表明，DEX治疗急性应激可影响NOX4/Nrf2/HO-1/NQO1信号通路，并抑制氧化应激。因此，DEX对急性应激引起的肾损伤具有保护作用，并在应激综合征中具有潜在的临床应用。

Dexmedetomidine Inhibits NOX4 and Alleviates Acute Stress-induced Renal Injury in Rats

This study was conducted to investigate the protective effects of dexmedetomidine (DEX) on renal injury caused by acute stress in rats and to explore the protective pathways of DEX on rat kidney from the perspective of oxidative stress. In this study, an acute restraint stress model was used, in which rats were forced to swim for 15 minutes and restrained for 3 hours. This experiment was performed with biochemical assays, histopathological section observation to assess renal function, followed by determination of oxidative stress and proteins of pathways related to oxidative stress. The open-field experiments confirmed that the acute stress model had been successfully established. DEX decreased NOX4 expression and increased Nrf2/HO-1/NQO1 expression, and the kidney biochemical results were significantly normalized in the DEX-treated group compared with the acute stress group, and the damage was significantly reduced in the pathological sections. The experimental results suggest that DEX treatment of acute stress can affect NOX4/Nrf2/HO-1/NQO1 signaling pathway and inhibit oxidative stress. Therefore, DEX has a protective effect on acute stress-induced renal injury and has potential clinical applications in stress syndromes.