fractalkine在持续低氧大鼠肺动脉重构氧化应激机制中的作用

摘要

Objective To explore the role of fractalkine in mechanisms of oxidative stress in pulmonary arterial remodeling in continuous hypoxia rats. Methods Eighteen male Spragiie-Dawley ( SD ) rats were divided into three groups: CH + NAC group ( CHI ), CH + NS group (CH2) and control group ( VC ). CH rats were subjected to hypoxia ( 10% ~12% 02for7h/d). CHI rats were injected N-acetylcysteine, and CH2 rats were injected equivalent NS. Results The levels of fractalkine, ROS and ability of inhibiting hydioxyl radicals in serum and the lung tissues in CHI group were statistically significant in comparison with CH2 and VC group( P <0. 05 ). Fraeta-lkine showed positive correlation with ROS , and showed negative correlation with ability of inhibiting hydioxyl radicals. There were significantly decreased in arterial wall thickness, WT% , and WA % of renal arteriole and pulmonary arteriole in CHI group in comparison with CH2 gioup, and there were significantly increased in CHI group in compaiison with VC group( P < 0. 05 ). Wall thickness of pulmonary arterioles, WT% and WA% showed positive conelation with frartalkine and ROS in pulmonaiy tissues, and showed negative correlation with ability of inhibiting hydioxyl radicals. Conclusion Fractalkine involved in the occurrence of pulmonary arterial remodeling in CH rats, and FKN may be one of the mechanisms of oxidative stress leading to pulmonaiy vascular remodeling.%目的 探讨fractalkine在持续低氧(CH)大鼠肺动脉重构氧化应激机制中的作用.方法 SD雄性大鼠18只按随机数字表法分为CH1、CH2和UC 3组.CH组舱内氧浓度保持10%~12%,7 h/d.CH1组给予NAC,CH2组予等量生理盐水.结果 CH1组血清及肺组织fractalkine、ROS、抑制羟自由基能力与CH2组及UC组比较差异有统计学意义(P<0.05);fractalkine与ROS正相关,与抑制羟自由基能力负相关.肺小动脉管壁厚度、WT%、WA%在CH1组较CH2组降低(P<0.05),较UC组升高(P<0.05).三者与肺组织fractalkine、ROS成正相关,与抑制羟自由基能力呈负相关.结论 fractalkine参与CH大鼠肺动脉重构的发生,fractalkine可能是氧化应激导致肺小动脉重构的机制之一.