角膜碱烧伤大鼠接受多西环素干预后的细胞凋亡情况及角膜和房水中IL-1、TNF-α、HIF-1α的表达

Effect of doxycycline intervention on the apoptosis as well as the IL-1,TNF-α and HIF-1α expression in cornea and aqueous humor in rats with corneal alkali burn

目的:研究多西环素干预对角膜碱烧伤大鼠细胞凋亡情况及角膜和房水中IL-1、TNF-α、HIF-1α表达量的影响。方法:选择雄性SD大鼠作为实验动物,随机分为对照组、碱烧伤组、多西环素组,氢氧化钠滴眼建立角膜碱烧伤模型后给予多西环素滴眼液滴眼干预。造模后14天和28天时,检测角膜中细胞凋亡分子、炎症反应细胞因子、血管新生分子的表达量以及房水中炎症反应细胞因子、血管新生分子的表达量。结果:造模后14天和28天时,碱烧伤组大鼠角膜组织中Bcl-2、PEDF的蛋白表达量显著低于对照组,Caspase-3、Caspase-8、Caspase-9、IL-1、TNF-α、HIF-1α、VEGF的蛋白表达量均显著高于对照组;多西环素大鼠角膜组织中Bcl-2、PEDF的蛋白表达量显著高于碱烧伤组,Caspase-3、Caspase-8、Caspase-9、IL-1、TNF-α、HIF-1α、VEGF的蛋白表达量均显著低于碱烧伤组。结论:多西环素用于角膜碱烧伤干预能够抑制细胞凋亡、炎症反应及血管新生。

Objective:To study the effect of doxycycline intervention on the apoptosis as well as the IL1,TNFαand HIF1αexpression in cornea and aqueous humor in rats with corneal alkali burn.Methods:Male SD rats were selected as experimental animals and randomly divided into control group,alkali burn group and doxycycline group,corneal alkali burn models were established by sodium hydroxide eye drop and then they received doxycycline eye drops intervention.The expression of apoptosis molecules,inflammatory response cytokines,angiogenesis moleculesin the cornea,the expression of inflammatory response cytokines and angiogenesis molecules in aqueous humor were detected14days and28days after model establishment.Results:Fourteen and twenty eight days after model establishment,Bcl2and PEDF protein expression in cornea tissue of alkali burn group was significantly lower than that of control group,while Caspase3,Caspase8,Caspase9,IL1,TNFα,HIF1αand VEGF protein expression was significantly higher than that of control group;Bcl2and PEDF protein expression in cornea tissue of doxycycline group was significantly higher than that of alkali burn group,while Caspase3,Caspase8,Caspase9,IL1,TNFα,HIF1αand VEGF protein expression was significantly lower than that of alkali burn group.Conclusion:Doxycycline for corneal alkali burn intervention can inhibit the apoptosis,inflammatory response and angiogenesis.