瑞芬太尼对缺氧复氧损伤人肝L02细胞的保护作用

Remifentanil protects L02 cells against anoxia/reoxygenation-induced injury

  • 摘要: 目的 探讨瑞芬太尼(remifentanil,REM)对缺氧复氧损伤人肝L02细胞的作用及机制。 方法 将培养的人肝L02细胞分为正常对照组(C组)、单纯缺氧复氧组(O组)及瑞芬太尼处理组(R组);其中R组又根据药物浓度不同分为7个亚组。C组正常培养,O、R两组缺糖缺氧处理5 h后恢复正常条件培养12 h,分别使用MTT比色法测定细胞活力、流式细胞仪检测细胞凋亡情况、比色法测定细胞培养液LDH活力,激光共聚焦显微镜观察细胞内钙浓度动态变化。 结果 5~40 ng/ml的瑞芬太尼处理使缺氧复氧损伤L02细胞活力上升、细胞凋亡比例下降,5~30 ng/ml的瑞芬太尼处理使培养液中LDH活力降低(P<0.05);40 ng/ml瑞芬太尼处理后L02细胞内钙浓度上升时间延迟(P<0.05)。 结论 5~40 ng/ml的瑞芬太尼处理对缺氧复氧损伤肝细胞具有保护作用,可能与瑞芬太尼抑制细胞凋亡和减轻钙超载有关。

     

    Abstract: Objective To study the role of remifentanil in protecting L02 cells against anoxia/reoxygenation-induced injury. Methods Cultured L02 cells were divided into normal control group (group C), anoxia/reoxygenation group (group O) and remifentanil treatment group(group R).Group R was further divided into 7 subgroups according to the different remifentanil concentrations.L02 cells in group C were normally cultured.L02 cells in groups O and R were exposed to anoxia for 5 hours followed by normal culture for 12 hours.The cell viability was assayed by MTT colorimetry, the cell apoptosis was detected by flow cytometry, and the LDH release from cells was measured by colorimetry.The dynamic changes of intracellular calcium concentration were observed under laser confocal microscope. Results The viability of anoxia/reoxygenation-injured L02 cells increased and the apoptosis of anoxia/reoxygenationinjured L02 cells decreased after they were treated with 5-40 ng/ml reminfentanil (P< 0.05).The LDH release from cells decreased after they were treated with 5-30 ng/ml reminfentanil (P< 0.05).The elevation of intracellular calcium concentration in anoxia/reoxygenation-injured L02 cells was delayed after treatment with 40 ng/ml reminfentanil (P< 0.05). Conclusion Reminfentanil at the concentration of 5-40 ng/ml can protect L02 cells against anoxia/reoxygenation-induced injury by inhibiting cell apoptosis and relieving calcium overload.

     

/

返回文章
返回