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Effect of dexmedetomidine on rats with renal ischemia-reperfusion injury and the expression of tight junction protein in kidney

机译:右美托咪定对肾缺血再灌注损伤大鼠的保护作用及肾脏紧密连接蛋白的表达

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摘要

To explore the protective effect of dexmedetomidine (Dex) on rats with renal ischemia-reperfusion injury and the influence of Dex on the expression of tight junction protein in kidney. Grouped 40 SPF male rats into 4 groups, sham operation group (group S), ischemia-reperfusion group (group I/R), pretreatment with Dex group (group Pre/Dex), post-treatment with Dex group (group Post/Dex), randomly, 10 rats each group. Rats in group S were anaesthetized and set up with removal of right kidney; rats in group I/R were set up with removal of right kidney and left renal artery clamping for 45 min followed by 60 min reperfusion; rats in group Pre/Dex were intravenous injected with Dex (1 μg/kg) for 30 min after indwelling catheter via femoral vein puncture; rats in group Post/Dex were intravenous injected with Dex (1 μg/kg) for 30 min after left renal reperfusion. The kidneys in each group were made out pathologic slices after 6 h I/R, stained with HE; blood samples were taken with separation plasma, creatinine (Scr) and urea nitrogen (BUN) were detected by automatic biochemical analyzer; IL-1β and TNF-α were detected by Enzyme-linked Immunosorbent Assay (ELISA); the expression level of tight junction protein ZO-1 and protein occludin in kidney were detected by Western-blot. The results of HE staining showed that, comparing to group S, the tissue of kidney in group I/R were damaged heavily with tubules dilatation and inflammation obviously, while lightened in group Pre/Dex and group Post/Dex. The results of detection of renal function and inflammatory factors showed that, comparing to group S, Scr, BUN, IL-1β and TNF-α were all enhanced in group I/R, group Pre/Dex and group Post/Dex, significantly (P < 0.05), while the inflammatory factors in group Pre/Dex and group Post/Dex were lower than in group I/R, significantly (P < 0.05). The results of Western-blot showed that the expression of protein ZO-1 and occludin in group Pre/Dex and group Post/Dex were higher than in group I/R, significantly (P < 0.05). Dex could reduce renal dysfunction induced by I/R, inhibit inflammatory response, up-regulate the expression of protein ZO-1 and occludin and protect renal.
机译:目的探讨右美托咪定(Dex)对肾脏缺血再灌注损伤大鼠的保护作用以及Dex对肾脏紧密连接蛋白表达的影响。将40只SPF雄性大鼠分为4组,假手术组(S组),缺血再灌注组(I / R组),Dex组预处理(Pre / Dex组),Dex组治疗后(Post / Dex组) ),每组随机10只。麻醉S组大鼠,取出右肾,将其麻醉。设置I / R组大鼠右肾和左肾动脉钳夹45分钟,再灌注60分钟。 Pre / Dex组的大鼠在留置导管后经股静脉穿刺静脉注射Dex(1μg/ kg)30分钟; Post / Dex组的大鼠在左肾再灌注后静脉注射Dex(1μg/ kg)30分钟。 I / R 6 h后,每组肾脏取病理切片,HE染色。分离血样,用自动生化分析仪检测肌酐(Scr)和尿素氮(BUN)。酶联免疫吸附法(ELISA)检测IL-1β和TNF-α。 Western blot检测肾脏中紧密连接蛋白ZO-1和闭合蛋白的表达水平。 HE染色结果显示,与S组相比,I / R组肾脏组织受到肾小管扩张和炎症的严重损害,而Pre / Dex组和Post / Dex组变轻。肾脏功能和炎性因子的检测结果表明,与S组相比,I / R组,Pre / Dex组和Post / Dex组的Scr,BUN,IL-1β和TNF-α均显着升高( P <0.05),而Pre / Dex组和Post / Dex组的炎症因子明显低于I / R组(P <0.05)。 Western-blot结果显示,Pre / Dex组和Post / Dex组蛋白ZO-1和occludin的表达均明显高于I / R组(P <0.05)。 Dex可以减轻I / R引起的肾功能不全,抑制炎症反应,上调ZO-1和occludin蛋白的表达并保护肾脏。

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