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:50μL 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 treatment also blocked astrocyte 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. 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 Intr alipid; 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 / 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 The ratio of Bcl-2 / Bax was 1.4, 0.8, and 0.6, and the Bcl-2 expression peak was at 72 hours (P <0.01) 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 0.01), with Bcl-2 / Bax ratios of 1.6-1.8 .ropofol treatment also blocked astrocyte proliferation and swelling. No apoptotic cells orBcl-2 / Bax expression was detected in astrocytes cultured in Hank’s or Intralipid solution. CONCLUSION: Propofol protects astrocytes by injury caused by hypoxia and reoxygenation via a mechanism that involves maintaining high ratios of Bcl-2 / Bax.