异氟醚预先给药对缺氧复氧诱发人脐静脉内皮细胞多配体蛋白聚糖-1脱落的影响

Effect of isoflurane pretreatment on hypooda/reoxygenation-induced syndecan-1 shedding from human umbilical vein endothelial cells

目的 探讨异氟醚预先给药对缺氧复氧诱发的人脐静脉内皮细胞（HUVECs）多配体蛋白聚糖．1脱落的影响。方法HUVECs培养于EMB-2培养液，采用随机数字表法，将其随机分为3组（n=32），正常对照组（C组）：密闭箱内逗人5％cq．95％02混合气体30min，在正常氧浓度下继续培养；缺氧，复氧组（H／R组）置于氧浓度为1％缺氧培养箱内孵育4h后，置于正常氧浓度的培养箱复氧2h；异氟醚预先给药组（I组）：密闭箱内通入1．73％异氟醚，30min后行细胞缺氧复氧，方法同H／R组。缺氧复氧结束时测定HUVECs多配体蛋白聚糖．1表达、培养液脱落多配体蛋白聚糖-1浓度、细胞渗透性和细胞活力。结果与C组比较，H／R组和I组培养液脱落多配体蛋白聚糖-1浓度和细胞渗透性升高，HUVECs多配体蛋白聚糖-1表达水平和细胞活力降低（P〈0．01）；与H／R组比较，I组培养液脱落多配体蛋白聚糖-1浓度和细胞渗透性降低，HUVECs多配体蛋白聚糖-1表达水平和细胞活力升高（P〈0．01）。结论异氟醚预先给药可通过抑制HUVECs多配体蛋白聚糖-1的脱落，从而减轻HUVECs缺氧复氧损伤。

Objective To investigate the effect of isoflurane pretreatment on hypoxia/reoxygenation （H/R）-indueed syndecan-1 shedding from hunan umbilical vein endothelial cells （HUVECs） .Methods HUVECs were cultured in EMB-2 medium and randorrly divided into 3 groups （ n = 32 each） ： control group （group C）, H/R group and isoflurane pretreatment group （group I）. H/R was produced by 4 h exposure of HUVECs to hypoxia followed by 2 h reoxygenation in H/R and I groups. HUVECs were exposed to the mixture of 5% CO2 and 95% O2 for 30 min and then cultured in normal cultme atmosphere （21% O2 ） in group C. In group I, HUVECs were exposed to 1.73% isoflurane and incubated for 30 min before H/R. The syndecan-1 expression, concentrations of shed syndecan-1 in the medium, and cell permeability and viability were measured at the end of reoxygenation. Resuits Compared with group C, the shed syrdecan-I concentration in the medium and cell permeability were significantly increased, while the syndecan-I expression and cell viability decreased in H/R and I groups （P 〈 0.01 ）. Compared with group H/R, the shed syndecan-1 concentration in the medium and cell permeability were significantly decreased, while the syndecan-1 expression and cell viability increased in group I （P 〈 0.01 ）. Conclusion Isoflurane pretreatment can protect HUVECs against H/R injury through inhibiting the syndecan-1 shedding.