摘要
目的研究不同浓度和时间七氟烷预处理对缺氧小鼠脑损伤的影响及可能机制。方法取40只C57BL/6J雄性小鼠,随机分为对照组(正常小鼠)、模型组(建立缺氧小鼠模型)、实验1组(建立缺氧小鼠模型+2%七氟烷预处理30 min)、实验2组(建立缺氧小鼠模型+4%七氟烷预处理30 min)、实验3组(建立缺氧小鼠模型+2%七氟烷预处理60 min),每组各8只。建立缺氧模型24 h后,观察各组小鼠脑组织海马CA1区形态学改变,比较各组血清乳酸脱氢酶(LDH)活性、脑组织谷胱甘肽过氧化物酶(GPx)和超氧化物歧化酶(SOD)活性及丙二醛含量、脑组织血管内皮生长因子(VEGF)和促红细胞生成素(EPO)的水平。结果经光镜下观察可见小鼠脑组织海马CA1区细胞水肿、固缩,且实验1、2、3组小鼠病理改变较模型组均明显减轻。模型组血清LDH活性较对照组明显升高(P<0.05)。实验1、2、3组血清LDH活性较模型组均明显下降(P<0.05),且以实验3组最为明显。模型组脑组织丙二醛含量较对照组明显升高,实验1、2、3组脑组织丙二醛含量较模型组均显著下降(P<0.05)。模型组和实验1、2组脑组织GPx活性较对照组均显著下降,实验3组脑组织GPx活性较模型组明显升高(P<0.05)。模型组和实验1、2、3组脑组织SOD活性较对照组均显著下降,且实验1、2、3组脑组织SOD活性较模型组均显著下降(P<0.05)。模型组脑组织VEGF和EPO的水平较对照组均明显升高(P<0.05)。实验1、2、3组脑组织VEGF和EPO的水平较对照组和模型组均明显下降(P<0.05),且以实验3组最为明显。结论通过七氟烷预处理可有效缓解缺氧导致的脑组织损伤,其作用机制可能与抑制氧化应激、调节抗缺氧蛋白合成密切相关,且2%七氟烷预处理60 min的效果更加明显。
Objective To study the effects of sevoflurane preconditioning at different concentrations and time on brain injury in hypoxic mice and its possible mechanism.Methods Forty C57BL/6J male mice were randomly divided into control group(normal mice),model group(hypoxic mice model),experimental group 1(hypoxic mice model+2%sevoflurane preconditioning for 30 min),experimental group 2(hypoxic mice model+4%sevoflurane preconditioning for 30 min),and experimental group 3(hypoxic mice model establishment+2%sevoflurane preconditioning for 60 min),8 rats in each group.Morphological changes of CA1 region in hippocampus of mice in each group were observed.Serum lactate dehydrogenase(LDH),glutathione peroxidase(GPx)and superoxide dismutase(SOD)activities,malondialdehyde content,vascular endothelial growth factor(VEGF)and erythropoietin(EPO)levels were compared in each group.Results 24 hours after the establishment of hypoxic model,the edema and contraction of hippocampal CA1 cells were observed under light microscopy,and the pathological changes of mice in groups 1,2 and 3 were significantly alleviated compared with the model group.The serum LDH activity in model group was significantly higher than that in control group(P<0.05).The LDH activity in serum of the experimental group 1,2 and 3 was significantly lower than that of the model group(P<0.05),especially in the experimental group 3.The content of malondialdehyde in brain tissue of model group was significantly higher than that of control group.The content of malondialdehyde in brain tissue of experiment 1,2 and 3 groups was significantly lower than that of model group(P<0.05).GPx activity in brain tissue of model group and experimental group 1 and 2 was significantly lower than that of control group.GPx activity in brain tissue of experimental group 3 was significantly higher than that of model group(P<0.05).SOD activity in brain tissue of model group and experimental group 1,2 and 3 was significantly lower than that of control group,and SOD activity in brain tissue of experimental group 1,2 and 3 was significantly lower than that of model group(P<0.05).The levels of VEGF and EPO in brain tissue of model group were significantly higher than those of control group(P<0.05).The levels of VEGF and EPO in brain tissue of experimental group 1,2 and 3 were significantly lower than those of control group and model group(P<0.05),especially in experimental group 3.Conclusion Sevoflurane preconditioning can effectively alleviate the brain injury caused by hypoxia.Its mechanism may be closely related to inhibiting oxidative stress and regulating the synthesis of anti-hypoxia proteins.The effect of 2%sevoflurane preconditioning for 60 minutes is more obvious.
作者
张伟
宋强
高成杰
ZHANG Wei;SONG Qiang;GAO Cheng-jie(Department of Anesthesiology,NO.960 Hospital of PLA,Jinan Shandong 250031,China)
出处
《临床和实验医学杂志》
2019年第20期2133-2136,共4页
Journal of Clinical and Experimental Medicine
基金
国家自然科学基金(编号:81501650)
关键词
小鼠
缺氧
脑损伤
七氟烷
预处理
氧化应激
Mice
Hypoxia
Brain injury
Sevoflurane
Preconditioning
Oxidative stress
