摘要
目的探讨氧化应激在视网膜脂质过氧化损伤发生机制中的作用。方法21 d出生的60只未成熟SD大鼠随机分为空气组和高氧组(每组30只)。空气组在空气中饲养;高氧组置于高浓度氧(95%)中饲养。ELISA方法检测大鼠血浆8-异-前列腺素F2α(8-iso-PGF2α)含量,透射电镜观察视网膜超微结构改变。结果在空气组,未成熟新生大鼠生后第3天、7天和14天血浆8-iso-PGF2α分别为19.09±5.57,18.24±5.91,17.00±5.58pg/mL,差异无显著性(F=1.024,P=0.3634);在高氧组,未成熟新生大鼠生后第3天、7天和14天血浆8-iso-PGF2α含量分别为28.33±5.59,51.20±15.01和84.54±14.85 pg/mL,差异具有显著性(F=150.7,P<0.01),并明显高于同一时间点空气组水平(t=2.863,P<0.05;t=5.073,P<0.01;t=11.006,P<0.01)。空气组未成熟大鼠的视网膜超微结构正常;高氧组未成熟新生大鼠在生后第3天视网膜超微结构即发生变化,表现为膜盘结构疏松、扭曲、断裂及线粒体显著肿胀等。结论氧化应激可导致未成熟视网膜脂质过氧化损伤,血浆8-iso-PGF2α水平升高与视网膜损伤程度相关。
Objective To investigate the role of oxidative stress in the pathogenesis of retinal injury induced by hyperoxia. Methods Sixty immature Sprague-Dawley （SD） rats, born at a gestational age of 21days, were randomly exposed to room air （air group, n =30） or 95% oxygen （hyperoxia group, n =30） immediately after birth. Plasma 8-isoprostaglandin F2α （ 8-iso-PGF2α ） levels were determined by ELISA. The uhrastructures of the retina were observed under a transmission electron microscope. Results The plasma 8-iso-PGF2α contents of the air group were 19.09 2 5.57, 18.24 2 5.91 and 17.00 2 5.58 pg/mL on the 3rd, 7th and 14th days after birth, respectively （ F = 1. 024, P 〉 0.05 ）. The plasma 8-iso-PGF2 contents in the hyperoxia group on the 3rd （28.33 25.59 pg/mL）, the 7th day （51.20 2 15.01 pg/ mL） and 14th day （ 84.54 2 14.85 pg/mL） after birth were significantly higher than those of the air group（ t = 2.863 ,P 〈 0.05 ;t = 5. 073, P 〈 0.01;t = 11. 006, P 〈 0.01 ）. Moreover, the plasma 8-iso-PGF2 contents in the hyperoxia group increased with the prolonged hyperoxia exposure （ F = 150.7, P 〈 0.01 ）. The uhrastroctures of retina in the air group were normal. Hyperoxia exposure resulted in abnormalities of the ultrastroctures of retina, manifesting as the membrane discs rarefied, twisted and disrupted and mitochondrial swelling. Conclusions Oxidative stress can results in retinal injury in immature rats. An increased plasma level of 8-iso-PGF2α is related to the injury degree of retina.
出处
《中国当代儿科杂志》
CAS
CSCD
2007年第2期174-176,共3页
Chinese Journal of Contemporary Pediatrics
基金
广东省医学科研基金(984182)
暨南大学自然科学基金(620008)资助
