七氟烷预处理抑制缺氧诱导的脑损伤
发布时间：2018-12-07 19:00
【摘要】：目的:观察七氟烷预处理对缺氧小鼠脑损伤的影响及其可能机制。方法:将60只雄性C57BL/6J小鼠,随机分为对照(C)组、缺氧(H)组、2%七氟烷预处理30 min组(S1+H组)、2%七氟烷预处理60 min组(S2+H组)和4%七氟烷预处理30 min组(S3+H组),每组10只。缺氧即持续吸入O2体积分数为(6.5±0.1)%的氮氧混合气体24 h构建缺氧模型;预处理即以O2体积分数为(21.0±0.5)%的氮氧混合气体为载气,分别吸入2%七氟烷30 min、2%七氟烷60 min和4%七氟烷30 min,洗脱15 min后进行缺氧处理。用光学显微镜及透射电子显微镜(TEM)观察海马CA1区形态学改变;比色法检测血清乳酸脱氢酶(LDH)活性;ELISA测定脑组织促红细胞生成素(EPO)和血管内皮生长因子(VEGF)含量;同时测定脑组织丙二醛(MDA)含量及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)活性。结果:缺氧24 h后,光镜下可见海马CA1区细胞水肿或固缩;各预处理组病理改变轻于H组。TEM下S2+H组细胞超微结构最为完整。H组血清LDH活性及脑组织EPO、VEGF、MDA含量显著高于C组,脑组织的SOD及GPx活性较C组明显降低。七氟烷预处理后血清LDH活性及脑组织EPO、VEGF含量较H组降低,以S2+H组最为显著;脑组织MDA含量及SOD活性降低,而GPx活性有所升高。结论:七氟烷预处理能减轻缺氧引起的脑组织损伤,其机制可能与调节抗缺氧蛋白合成及降低氧化应激有关。
[Abstract]:Aim: to observe the effect of sevoflurane preconditioning on brain injury in hypoxic mice and its possible mechanism. Methods: sixty male C57BL/6J mice were randomly divided into control (C) group, hypoxic (H) group and 2% sevoflurane pretreated 30 min group (S 1H group). 10 rats were pretreated with 2% sevoflurane for 60 min (S 2H group) and 4% sevoflurane for 30 min (S3H group). Hypoxia model was established by inhaling oxygen (6.5 卤0.1)% nitrogen and oxygen mixture for 24 h. The oxygen mixture of (21.0 卤0.5)% oxygen and nitrogen was used as carrier gas. After inhalation of 2% sevoflurane for 30 min,2%, sevoflurane for 60 min and 4% sevoflurane for 30 min, for 15 min, anoxic treatment was performed. The morphological changes of hippocampal CA1 were observed by optical microscope and transmission electron microscope (TEM), and the activity of lactate dehydrogenase (LDH) in serum was detected by colorimetric method. The contents of erythropoietin (EPO) and vascular endothelial growth factor (VEGF), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured by ELISA. Results: after 24 hours of hypoxia, edema or pyknosis were observed in the CA1 area of hippocampus under light microscope. The ultrastructure of S 2H group was the most complete under TEM. The activity of serum LDH and the content of EPO,VEGF,MDA in brain tissue in H group were significantly higher than those in group C, and the activities of SOD and GPx in brain tissue were significantly lower than those in group C. After sevoflurane preconditioning, the activity of serum LDH and the content of EPO,VEGF in brain tissue were lower than those in group H, especially in group S 2H, and the contents of MDA and SOD in brain tissue decreased, but the activity of GPx increased. Conclusion: sevoflurane pretreatment can attenuate the brain tissue damage induced by hypoxia, and its mechanism may be related to the regulation of anti-hypoxia protein synthesis and the reduction of oxidative stress.
【作者单位】： 暨南大学附属第一医院麻醉科;
【基金】：广东省自然科学基金资助项目(No.2017A30313514) 围术期口服多功能液体的研发及其临床前研究(No.2017ZC0012)
【分类号】：R614
[Abstract]:Aim: to observe the effect of sevoflurane preconditioning on brain injury in hypoxic mice and its possible mechanism. Methods: sixty male C57BL/6J mice were randomly divided into control (C) group, hypoxic (H) group and 2% sevoflurane pretreated 30 min group (S 1H group). 10 rats were pretreated with 2% sevoflurane for 60 min (S 2H group) and 4% sevoflurane for 30 min (S3H group). Hypoxia model was established by inhaling oxygen (6.5 卤0.1)% nitrogen and oxygen mixture for 24 h. The oxygen mixture of (21.0 卤0.5)% oxygen and nitrogen was used as carrier gas. After inhalation of 2% sevoflurane for 30 min,2%, sevoflurane for 60 min and 4% sevoflurane for 30 min, for 15 min, anoxic treatment was performed. The morphological changes of hippocampal CA1 were observed by optical microscope and transmission electron microscope (TEM), and the activity of lactate dehydrogenase (LDH) in serum was detected by colorimetric method. The contents of erythropoietin (EPO) and vascular endothelial growth factor (VEGF), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured by ELISA. Results: after 24 hours of hypoxia, edema or pyknosis were observed in the CA1 area of hippocampus under light microscope. The ultrastructure of S 2H group was the most complete under TEM. The activity of serum LDH and the content of EPO,VEGF,MDA in brain tissue in H group were significantly higher than those in group C, and the activities of SOD and GPx in brain tissue were significantly lower than those in group C. After sevoflurane preconditioning, the activity of serum LDH and the content of EPO,VEGF in brain tissue were lower than those in group H, especially in group S 2H, and the contents of MDA and SOD in brain tissue decreased, but the activity of GPx increased. Conclusion: sevoflurane pretreatment can attenuate the brain tissue damage induced by hypoxia, and its mechanism may be related to the regulation of anti-hypoxia protein synthesis and the reduction of oxidative stress.
【作者单位】： 暨南大学附属第一医院麻醉科;
【基金】：广东省自然科学基金资助项目(No.2017A30313514) 围术期口服多功能液体的研发及其临床前研究(No.2017ZC0012)
【分类号】：R614
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