Propofol blocks apoptosis and Bcl-2 and Bax expression induced by hypoxia-reoxygenation in primary cultures of rat hippocampal astrocytes  被引量:3

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

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作  者:Qing Li Juying Liu Long Zhou Chengming Qin 

机构地区:[1]Department of Anesthesiology, Taihe Hospital of Yunyang Medical Coflege, Shiyan 442000, Hubei Province, China

出  处:《Neural Regeneration Research》2009年第7期518-522,共5页中国神经再生研究(英文版)

摘  要: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, wJth 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; 50 μL 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 (250 μmol/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 Bct-2 and Bax expression (P 〈 0.05, P 〈 0.01), with Bcl-2/Bax ratios of 1.6-1.8. Propofol treatmenBACKGROUND: 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, wJth 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; 50 μL 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 (250 μmol/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 Bct-2 and Bax expression (P 〈 0.05, P 〈 0.01), with Bcl-2/Bax ratios of 1.6-1.8. Propofol treatmen

关 键 词:PROPOFOL hippocampal astrocyte APOPTOSIS hypoxia and re-oxygenation BCL-2 BAX 

分 类 号:Q421[生物学—神经生物学] Q255[生物学—生理学]

 

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