二氧化铈纳米颗粒对大鼠心肌缺血再灌注损伤的保护作用
Protective effects of CeO2 nanoparticles on the myocardial ischemia-reperfusion injury in rats
摘要目的 观察二氧化铈(CeO2)纳米颗粒对大鼠心肌缺血再灌注损伤的保护作用.方法 将SD大鼠50只随机分为假手术组、模型组、1~ 10 nm粒径组、10 ~ 25 nm粒径组、50 nm粒径组,每组10只,制作缺血再灌注模型.采用黄嘌呤氧化酶法和比色法分别测定超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,硫代巴比妥酸法测定丙二醛(MDA)含量,同时观察心肌组织病理学和细胞凋亡.结果 与假手术组比较,模型组SOD、GSH-Px活性明显下降,MDA含量明显升高(P<0.05);与模型组比较,3种不同粒径组SOD、GSH-Px活性明显升高,MDA含量明显降低(P<0.05).3种不同粒径组心肌细胞凋亡指数[1 ~ 10 nm组:(21.00 ±3.90)%;10~25 nm组:(16.38±3.59)%;50 nm组:(24.20±5.88)%]与模型组[(32.92±7.46)%]比较明显降低(P<0.05).结论 二氧化铈纳米颗粒能减轻大鼠缺血再灌注心肌的氧化应激,具有较好的心肌保护作用.
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abstractsObjective To investigate the protective effects of cerium oxide (CeO2) nanoparticles on myocardial ischemia-reperfusion injury in rats.Methods Fifty male Sprague-Dawley rats were randomly divided into five groups:sham group,experimental group and three preconditioning groups with different particle diameter [1-10 nm group,10-25 nm group and 50 nm group (n =10 in each group)].The myocardial ischemia-reperfusion model was established successfully.The activities of superoxide dismutase (SOD) and glutathione (GSH)-Px,and the content of malondialdehyde (MDA) in myocardial tissue were determined.The morphology of myocardium was observed under a light microscope,and the apoptosis of myocardial cells was detected by using TdT-mediated dUTP nick end labeling (TUNEL) method.Results As compared with the Sham group,the activities of SOD and GSH-Px in experimental group were significantly decreased (P < 0.05),while the content of MDA was increased (P < 0.05).The activities of SOD and GSH-Px were increased and the content of MDA was decreased in the three different particle diameter groups as compared with the experimental group (P < 0.05).The apoptosis of myocardial cells was significantly decreased in the three different particle diameter groups [(21.00 ± 3.90)% for 1-10 nm group; (16.38 ± 3.59)% for 10-25 nm group; and (24.20 ± 5.88)% for 50 nm group] as compared the experimental group [(32.92 ± 7.46) %] (P < 0.05).Conclusion The CeO2 nanoparticles can protect the myocardium from ischemia-reperfusion injury by attenuating oxidative stress.
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