Liu Yun-En, Tong Chang-Ci, Zhang Yu-Biao, Jin Hong-Xu, Gao Yan, Hou Ming-Xiao
Department of Emergency Medicine, Laboratory of PLA Wound and Trauma Center, The General Hospital of Shenyang Military District, PLA Shenyang 110016, China.
Int J Clin Exp Med. 2015 Oct 15;8(10):18751-7. eCollection 2015.
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.
探讨右美托咪定（Dex）对肾缺血再灌注损伤大鼠的保护作用及对肾脏紧密连接蛋白表达的影响。将40只SPF级雄性大鼠随机分为4组，假手术组（S组）、缺血再灌注组（I/R组）、Dex预处理组（Pre/Dex组）、Dex后处理组（Post/Dex组），每组10只。S组大鼠麻醉后行右肾切除术；I/R组大鼠行右肾切除术并夹闭左肾动脉45分钟，再灌注60分钟；Pre/Dex组大鼠经股静脉穿刺留置导管后30分钟静脉注射Dex（1μg/kg）；Post/Dex组大鼠左肾再灌注后30分钟静脉注射Dex（1μg/kg）。缺血再灌注6小时后取各组大鼠肾脏制作病理切片，HE染色；采集血样分离血浆，用自动生化分析仪检测肌酐（Scr）和尿素氮（BUN）；采用酶联免疫吸附测定法（ELISA）检测白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）；采用蛋白质免疫印迹法检测肾脏紧密连接蛋白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组肾脏组织损伤严重，肾小管扩张、炎症明显，而Pre/Dex组和Post/Dex组损伤减轻。肾功能及炎症因子检测结果显示，与S组相比，I/R组、Pre/Dex组和Post/Dex组的Scr、BUN、IL-1β和TNF-α均显著升高（P<0.05），而Pre/Dex组和Post/Dex组的炎症因子低于I/R组，差异有统计学意义（P<0.05）。蛋白质免疫印迹法结果显示，Pre/Dex组和Post/Dex组的ZO-1和闭合蛋白表达高于I/R组，差异有统计学意义（P<0.05）。Dex可减轻I/R诱导的肾功能障碍，抑制炎症反应，上调ZO-1和闭合蛋白的表达，保护肾脏。
