文献类型： 外文期刊
作者： Yang, Haotian 1 ; Chen, Yongping 1 ; Wang, Zhiqiang 1 ; Huang, Yuxiang 1 ; Ma, Zhigang 1 ; Zou, Yue 1 ; Dong, Jiaqiang 1 ; Zhang, Hong 1 ; Huo, Mingdong 1 ; Lv, Mingzhe 1 ; Liu, Xuesong 1 ; Zhang, Guohua 1 ; Wang, Shuang 1 ; Yang, Kun 1 ; Zhong, Peng 1 ; Jiang, Botao 1 ; Kou, Yuhong 1 ; Chen, Zhifeng 1 ;
作者机构： 1.HeiLongJiang Acad Agr Sci, Branch Anim Husb & Vet, Qiqihar City 161005, Heilongjiang, Peoples R China
关键词： acute stress; oxidative stress; kidney injury; dexmedetomidine; NOX4
期刊名称：JOURNAL OF PHARMACY AND PHARMACOLOGY （ 影响因子：3.3； 五年影响因子：3.7 ）
ISSN： 0022-3573
年卷期： 2024 年
页码：
收录情况： SCI
摘要： Objectives The study aimed to investigate the protective effects of dexmedetomidine (DEX) on renal injury caused by acute stress in rats and explore the protective pathways of DEX on rat kidneys in terms of oxidative stress. Methods An acute restraint stress model was utilized, where rats were restrained for 3 hours after a 15-minute swim. Biochemical tests and histopathological sections were conducted to evaluate renal function, along with the measurement of oxidative stress and related pathway proteins. Key findings The open-field experiments validated the successful establishment of the acute stress model. Acute stress-induced renal injury led to increased NADPH oxidase 4 (NOX4) protein expression and decreased expression levels of nuclear transcription factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H: quinone oxidoreductase 1 (NQO1). Following DEX treatment, there was a significant reduction in renal NOX4 expression. The DEX-treated group exhibited normalized renal biochemical results and less damage observed in pathological sections compared to the acute stress group. Conclusions The findings suggest that DEX treatment during acute stress can impact the NOX4/Nrf2/HO-1/NQO1 signaling pathway and inhibit oxidative stress, thereby preventing acute stress-induced kidney injury. Additionally, DEX shows promise for clinical applications in stress syndromes.
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