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目的探讨水通道蛋白亚型3(aquaporin 3,Aqp3)在脓毒症肺血管通透性中的作用及SS-31对其的影响。方法采用SD大鼠盲肠结扎穿孔复制脓毒症模型。在整体动物水平上分为假手术组,脓毒症6、12 h组,在离体细胞水平分为空白对照组,LPS刺激6、12 h组,分别观察脓毒症和脂多糖(lipopolysaccharide,LPS)刺激6、12 h后肺静脉Aqp3的表达和血管通透性的变化,以及干扰Aqp3后内皮细胞通透性的变化。进一步观察抗氧化剂SS-31对Aqp3的表达与血管通透性的作用。结果脓毒症和LPS刺激内皮细胞后Aqp3表达和肺血管通透性均明显增加,与假手术组和空白对照组比较差异有统计学意义(P<0.05)。用RNAi抑制Aqp3的表达,可明显拮抗由LPS刺激引起的内皮细胞通透性增加,与LPS刺激组相比差异有统计学意义(P<0.05)。在整体动物和离体细胞水平应用抗氧化剂SS-31均可降低由脓毒症和LPS刺激引起的Aqp3表达和血管通透性的增加,与脓毒症和LPS刺激组比较差异有统计学意义(P<0.05)。结论 Aqp3参与了脓毒症肺血管通透性的调节,抗氧化措施可降低脓毒症肺血管通透性及下调Aqp3的表达。
Objective To investigate the role of aquaporin 3 (Aqp3) in pulmonary vascular permeability induced by sepsis and the effect of SS-31 on it. Methods SD cecal ligation and perforation were used to replicate sepsis model. At the level of whole animal, the animals were divided into sham-operation group, sepsis group at 6 and 12 h, divided into blank control group and LPS-stimulated group at 6 and 12 h, respectively. Sepsis and lipopolysaccharide LPS) for 6 and 12 h, the expression of Aqp3 in pulmonary vein and the changes of vascular permeability, as well as the change of endothelial cell permeability after interference with Aqp3. The effect of anti-oxidant SS-31 on Aqp3 expression and vascular permeability was further observed. Results Aqp3 expression and pulmonary vascular permeability were significantly increased in sepsis and LPS-stimulated endothelial cells, which were significantly different from those in sham operation group and blank control group (P <0.05). Inhibition of Aqp3 expression by RNAi significantly antagonized the increase of endothelial cell permeability induced by LPS stimulation compared with LPS stimulation group (P <0.05). Antioxidant SS-31 could reduce the expression of Aqp3 and the increase of vascular permeability induced by sepsis and LPS stimulation in both whole animal and ex vivo cells, which was significantly different from that of sepsis and LPS stimulation group (P <0.05). Conclusions Aqp3 is involved in the regulation of pulmonary vascular permeability in sepsis. Antioxidant actions may reduce the pulmonary vascular permeability and down-regulate the expression of Aqp3 in sepsis.