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| 右美托咪定减轻肾缺血-再灌注损伤中肾小球内皮糖萼的破坏 |
| Dexmedetomidine preserves glomerular endothelial glycocalyx during kidney ischemia-reperfusion injury in rats |
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| DOI：10.12089/jca.2019.06.014 |
| 中文关键词: 右美托咪定 肾小球内皮糖萼 缺血-再灌注损伤 乙酰肝素酶1 血管紧张素受体2 |
| 英文关键词: Dexmedetomidine Glomerular endothelial glycocalyx Ischemia-reperfusion injury Heparanase-1 Tie2 |
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| 中文摘要: |
目的 观察右美托咪定对肾缺血-再灌注损伤（kidney ischemia-reperfusion injury，KIRI）中肾小球内皮糖萼的影响。
方法 成年雄性SD大鼠28只，随机分为四组：假手术组(S组)、假手术+右美托咪定组（SD组）、肾缺血-再灌注组(R组)和肾缺血-再灌注+右美托咪定组（RD组），每组7只。术前30 min SD组和RD组腹腔注射右美托咪定25 μg/kg，S组和R组注射等体积生理盐水。S组和SD组进行假手术，R组和RD组建立缺血45 min再灌注24 h急性肾损伤模型。24 h后分别检测血肌酐（Scr）、血尿素氮（BUN）浓度及观察肾组织的病理学变化。电镜和共聚焦显微镜下观察肾小球内皮糖萼的结构变化。采用Western blot法测定肾组织多配体聚糖1（Syndecan-1）、乙酰肝素酶1（Heparanase-1）、血管生成素受体2（Tie2）蛋白含量。
结果 与S组比较，R组Scr和BUN浓度明显升高（P<0.05），肾组织病理性损伤明显加重，电镜和共聚焦显微镜下肾小球内皮糖萼结构明显破坏，肾组织Syndecan-1、Tie2蛋白含量明显降低（P<0.05），Heparanase-1蛋白含量明显升高（P<0.05）。与R组比较，RD组Scr和BUN浓度明显降低（P<0.05），肾组织病理性损伤明显减轻，电镜和共聚焦显微镜下肾小球内皮糖萼结构破坏明显减轻，肾组织Syndecan-1、Tie2蛋白含量明显升高（P<0.05），Heparanase-1蛋白含量明显降低（P<0.05）。
结论 右美托咪定可能通过保护和重建肾小球内皮糖萼减轻KIRI，其机制可能与抑制Heparanase-1以及激活Tie2受体有关。 |
| 英文摘要: |
Ojective To observe the effect of dexmedetomidine on glomerular endothelial glycocalyx during kidney ischemia-reperfusion injury in rats.
Methods Twenty eight adult male Sprague-Dawley rats were randomly divided into four groups (n = 7 each): sham group (group S), sham + dexmedetomidine group (group SD), ischemia-reperfusion group (group R) and ischemia-reperfusion + dexmedetomidine group (group RD). Dexmedetomidine was intraperitoneally injected with a dose of 25 μg/kg 30 min before operation in groups SD and RD, and the same volume of saline was injected in groups S and R, respectively. Sham operation was conducted in groups S and SD, and 45 min of ischemia followed by 24 h reperfusion in groups R and RD. After 24 h，levels of serum creatinine (Scr) and blood urea nitrogen (Bun) and kidney tissue histopathology were evaluated. The glomerular endothelial glycocalyx was visualized by transmission electron microscopy and confocal microscopy. Levels of Syndecan-1, Heparanase-1 and Tie2 were measured in kidney tissues.
Results Compared with group S, blood Scr and BUN were significantly increased (P < 0.05), kidney tissue histopathological injury was significantly aggravated, the structure of the glomerular endothelial glycocalyx was significantly damaged under electronic microscopy and confocal microscopy, the expression levels of Syndecan-1 and Tie2 in kidney tissue were significantly decreased (P < 0.05), and the expression level of Heparanas-1 was significantly increased in group R (P < 0.05). Compared with group R, blood Scr and BUN were significantly reduced (P < 0.05), kidney tissue histopathology injury was significantly alleviated, the structure destruction of the glomerular endothelial glycocalyx was significantly reduced under electronic microscopy and confocal microscopy, the expression levels of Syndecan-1 and Tie2 in kidney tissue were significantly increased (P < 0.05), and the expression level of Heparanase-1 was significantly reduced in group RD (P < 0.05).
Conclusion Dexmedetomidine-pretreatment attenuates kidney ischemia-reperfusion injury in rats possibly through protecting and restoring the glomerular endothelial glycocalyx. The renoprotective effects are probably related to Heparanase-1 inhibition and Tie2 activation. |
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