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首页 > 中国神经再生研究(英文版) >Propofol blocks apoptosis and Bcl-2 and Bax expression induced by hypoxia-reoxygenation in primary cultures of rat hippocampal astrocytes

Propofol blocks apoptosis and Bcl-2 and Bax expression induced by hypoxia-reoxygenation in primary cultures of rat hippocampal astrocytes

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BACKGROUND: Cerebral hippocampal astrocytes are more sensitive.to ischemic injury than neurons. Hypoxic-ischemic brain injury induces profound astrocyte apoptosis, and propofol may protect against astrocyte apoptosis.OBJECTIVE: To verify the protective effects of propofol against astrocyte apoptosis and to investigate anti-apoptotic Bcl-2 and pro-apoptotic Bax expression in primary cultures of rat hippocampal astrocytes exposed to hypoxia-reoxygenation for different periods of time following propofol treatment.DESIGN, TIME, AND SETTING: In vitro neural immunocytochemistry was performed at the Central Laboratory of Yunyang Medical College between September 2007 and March 2008.MATERIALS: A total of 30 Wistar rats, aged 1-3 days, with equal numbers of males and females,were included for isolation and culture of hippocampal astrocytes.METHODS: Hippocampal astrocytes were purified and cultured for 3 weeks and treated with four culture conditions: 50 μL Hank's solution (normal control); 0.2 mL/L Intralipid; 50μL Hank's solution for 10 minutes followed by hypoxic incubation for 4 hours and normoxic incubation for 12, 24, 36, 48,60 or 72 hours; propofol (250μmol/L final) for 10 minutes followed by hypoxic incubation for 4 hours and normoxic incubation for 12, 24, 36, 48, 60 and 72 hours.MAIN OUTCOME MEASURES: (1) Morphologic changes in hippocampal astrocytes. (2) Levels of astrocyte apoptosis and Bcl-2 and Bax expression.RESULTS: Hypoxia and reoxygenation increased apoptosis over time, with Bcl-2 expression peaking at 24 hours and decreasing gradually (P<0.01); Bax expression peaked at 72 hours (P<0.01 ); the ratio of Bcl-2/Bax was 1.4, 0.8, and 0.6, respectively, at 24, 48 and 72 hours.Non-apoptotic astrocytes showed significant proliferation and swelling. Propofol treatment decreased apoptosis after hypoxia-reoxygenation (P<0.01), as well as Bcl-2 and Bax expression (P<0.05, P<0.01), with Bcl-2/Bax ratios of 1.6-1.8. Propofol treatmentalso blocked astrecyte proliferation and swelling. No apoptotic cells or Bcl-2/Bax expression was detected in astrocytes cultured in Hank's or Intralipid solution.CONCLUSION: Propofol protects astrocytes against injury caused by hypoxia and reoxygenation via a mechanism that involves maintaining high ratios of Bcl-2/Bax.

作 者 Qing Li(Department of Anesthesiology,Taihe Hospital of Yunyang Medical College,Shiyan 442000,Hubei Province,China);Juying Liu(Department of Anesthesiology,Taihe Hospital of Yunyang Medical College,Shiyan 442000,Hubei Province,China);Long Zhou(Department of Anesthesiology,Taihe Hospital of Yunyang Medical College,Shiyan 442000,Hubei Province,China);Chengming Qin(Department of Anesthesiology,Taihe Hospital of Yunyang Medical College,Shiyan 442000,Hubei Province,China);
刊 名 中国神经再生研究(英文版)  2009年4卷07期 518-522页  科学引文索引扩展版(SCI Expanded)收录美国生物学预评数据库(BIOSIS Previews)收录美国《化学文摘》(Chemical Abstracts)收录
英文期刊名 NEURAL REGENERATION RESEARCH
关键词 propofol hippocampal astrocyte apoptosis hypoxia and re-oxygenation Bcl-2 Bax
分类号 R74
DOI号 10.3969/j.issn.1673-5374.2009.07.007

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