七氟烷預處理抑制缺氧誘導的腦損傷
發(fā)布時間：2018-12-07 19:00
【摘要】：目的:觀察七氟烷預處理對缺氧小鼠腦損傷的影響及其可能機制。方法:將60只雄性C57BL/6J小鼠,隨機分為對照(C)組、缺氧(H)組、2%七氟烷預處理30 min組(S1+H組)、2%七氟烷預處理60 min組(S2+H組)和4%七氟烷預處理30 min組(S3+H組),每組10只。缺氧即持續(xù)吸入O2體積分數(shù)為(6.5±0.1)%的氮氧混合氣體24 h構建缺氧模型;預處理即以O2體積分數(shù)為(21.0±0.5)%的氮氧混合氣體為載氣,分別吸入2%七氟烷30 min、2%七氟烷60 min和4%七氟烷30 min,洗脫15 min后進行缺氧處理。用光學顯微鏡及透射電子顯微鏡(TEM)觀察海馬CA1區(qū)形態(tài)學改變;比色法檢測血清乳酸脫氫酶(LDH)活性;ELISA測定腦組織促紅細胞生成素(EPO)和血管內皮生長因子(VEGF)含量;同時測定腦組織丙二醛(MDA)含量及超氧化物歧化酶(SOD)和谷胱甘肽過氧化物酶(GPx)活性。結果:缺氧24 h后,光鏡下可見海馬CA1區(qū)細胞水腫或固縮;各預處理組病理改變輕于H組。TEM下S2+H組細胞超微結構最為完整。H組血清LDH活性及腦組織EPO、VEGF、MDA含量顯著高于C組,腦組織的SOD及GPx活性較C組明顯降低。七氟烷預處理后血清LDH活性及腦組織EPO、VEGF含量較H組降低,以S2+H組最為顯著;腦組織MDA含量及SOD活性降低,而GPx活性有所升高。結論:七氟烷預處理能減輕缺氧引起的腦組織損傷,其機制可能與調節(jié)抗缺氧蛋白合成及降低氧化應激有關。
[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 鹵0.1)% nitrogen and oxygen mixture for 24 h. The oxygen mixture of (21.0 鹵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.
【作者單位】： 暨南大學附屬第一醫(yī)院麻醉科;
【基金】：廣東省自然科學基金資助項目(No.2017A30313514) 圍術期口服多功能液體的研發(fā)及其臨床前研究(No.2017ZC0012)
【分類號】：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 鹵0.1)% nitrogen and oxygen mixture for 24 h. The oxygen mixture of (21.0 鹵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.
【作者單位】： 暨南大學附屬第一醫(yī)院麻醉科;
【基金】：廣東省自然科學基金資助項目(No.2017A30313514) 圍術期口服多功能液體的研發(fā)及其臨床前研究(No.2017ZC0012)
【分類號】：R614
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