摘要/Abstract

摘要： 目的·检测丙泊酚对大鼠海马星形胶质细胞的影响，并探讨其作用机制。方法·根据丙泊酚注射时间，24只SD大鼠随机分为即时（0 min）组、45 min组和90 min组，每组8只。丙泊酚注射液（10 mg/mL）以100 mg/kg腹腔注射后，用定量PCR检测大鼠海马胶质纤维酸性蛋白（glial fibrillary acidic protein，GFAP）和S100β的mRNA水平。体外培养原代大鼠海马星形胶质细胞，并用10 μmol/L细胞外信号调节激酶（extracellular signal-regulated kinase，ERK）抑制剂PD98059预处理细胞2 h（不加抑制剂为对照），随后用10 μmol/L丙泊酚孵育24 h，检测细胞活力及GFAP表达。结果·丙泊酚腹腔注射后45 min、90 min，海马组织中GFAP的mRNA水平分别是注射即刻（0 min）的（1.32±0.12）倍（P0.000）和（1.12±0.09）倍（P0.012），S100β的mRNA水平分别是注射即刻（0 min）的（1.14±0.11）倍（P0.005）和（1.05±0.10）倍（P0.284）；而且，GFAP和S100β的mRNA水平均呈时程依赖性变化，先增高，而后降低。体外实验显示，丙泊酚显著提高原代海马星形胶质细胞的细胞活力（P0.041）和GFAP的mRNA水平（P0.026），但是丙泊酚的此作用可被ERK抑制剂PD98059逆转。结论·丙泊酚通过ERK信号通路时程依赖性地上调海马星形胶质细胞GFAP和S100β的表达，激活胶质细胞。
关键词: 丙泊酚, 胶质纤维酸性蛋白, S100&, beta, 星形胶质细胞, 细胞外信号调节激酶
Abstract:
Objective · To detect the effects of propofol on rat hippocampal astrocytes and clarify its mechanism. Methods · According to the time after propofol injection, twenty-four SD rats were randomly divided into three groups, i.e. 0 min, 45 min and 90 min group. Rats were administrated intraperitoneally with propofol (10 mg/mL, 100 mg/ kg body weight). The levels of glial fibrillary acidic protein (GFAP) and S100β mRNA in rat hippocampus were evaluatedrealtime PCR. And cell viabilities and levels of GFAP mRNA were examined in primary cultured hippocampal astrocytes induced10 μmol/L propofol with or without 10 μmol/L extracellular signal-regulated kinase (ERK) inhibitor PD98059 pretreatment. Results · The mRNA levels of GFAP in the hippocampal tissue were (1.32±0.12) times (P0.000) and (1.12±0.09) times (P0.012) that in 0 min group, respectively,45 min and 90 min after injection of propofol. The mRNA levels of S100βin the hippocampal tissue were (1.14±0.11) times (P0.005) and (1.05±0.10)times (P0.284) that in 0 min group, respectively, 45 min and 90 min after injection of propofol. The mRNA levels of GFAP and S100β were time-dependently altered, first increasing, and then decreasing. In vitro, the cell viabilities (P0.041) and levels of GFAP mRNA (P0.026) in primary cultured hippocampal astrocytes were significantly elevated after propofol treatment, and these effects of propofol were reversedERK inhibitor PD98059.Conclusion · Propofol time-dependently upregulated the of GFAP and S100βvia ERK signaling pathway in rat hippocampal astrocytes, so as to activate astrocytes.
Key words: propofol, glial fibrillary acidic protein (GFAP), S100&, beta, astrocyte, extracellular signal-regulated kinase (ERK)


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