低氧环境下丙泊酚致PC12细胞损伤的机制研究

发布时间：2018-03-11 20:54

本文选题：丙泊酚　切入点：低氧　出处：《重庆医科大学》2017年硕士论文　论文类型：学位论文

【摘要】：目的丙泊酚是临床麻醉最常用的静脉麻醉药之一,丙泊酚的反复应用可引起神经细胞凋亡增加,损伤学习、记忆、认知功能,低氧是围手术期容易被忽略的并发症,也是引起细胞凋亡、认知功能障碍的重要因素之一。本研究以神经元样PC12细胞为研究对象,从氧化应激角度对低氧环境下丙泊酚对PC12细胞株凋亡的影响及机制进行探讨,为有效干预麻醉手术后并发症的发生及术后认知功能障碍的治疗提供新的思路。方法将PC12细胞接种于培养板中,采用随机数字表法,将其随机分为6组:丙泊酚低氧组(PH组)、丙泊酚空气组(PA组)和丙泊酚氧气组(PO组),丙泊酚浓度为10μM。低氧对照组(CH组)、空气对照组(CA组)和氧气对照组(CO组)。药物处理完毕后分别放入低氧(5%O2),空气和氧气(35%O2)环境的细胞培养箱培养,8小时后进行流式检测细胞凋亡情况,检测细胞内ROS水平和细胞SOD酶活力。结果(1)MTT分析发现,丙泊酚10μM干预8h对PC12细胞的增殖有明显抑制作用(P0.05)。(2)丙泊酚处理组凋亡率均大于各对照组,且PH组凋亡率大于PA及PO组,差异具有统计学意义(P0.05)。(3)各丙泊酚处理组PA、PO、PH组,较各对照组CA、CO、CH组,ROS水平均有升高;并且PH组较PA、PO组,ROS生成水平明显升高。(4)与CA、CO、CH组相比,各PA、PO、PH中SOD表达明显增加(P0.05),PH组SOD水平较PA及PO组显著增加(P0.05)。结论本研究初步证实低氧环境下丙泊酚可通过氧化应激损伤导致神经元样PC12细胞凋亡增加,但其具体机制仍需我们进一步的研究。
[Abstract]:Objective propofol is one of the most commonly used intravenous anesthetics in clinical anaesthesia. The repeated use of propofol can induce increased neuronal apoptosis, impaired learning, memory, cognitive function and hypoxia, which are easily neglected complications during perioperative period. It is also one of the important factors to induce apoptosis and cognitive dysfunction. In this study, we investigated the effect and mechanism of propofol on apoptosis of PC12 cell line in hypoxic environment from the perspective of oxidative stress in neuron-like PC12 cells. Methods PC12 cells were inoculated into the culture plate, and the random number table method was used. They were randomly divided into 6 groups: propofol hypoxia group (PH group), propofol air group (PA group), propofol oxygen group (10 渭 m) and propofol concentration (10 渭 m). After the treatment, the cells were cultured in a cell incubator in hypoxia 5o 2, air and oxygen 35 O 2, respectively. After 8 hours of culture, the apoptosis of cells was detected by flow cytometry. The level of ROS and the activity of SOD enzyme were measured. Results the results showed that propofol (10 渭 M) inhibited the proliferation of PC12 cells significantly for 8 h.) the apoptotic rate of propofol treated group was higher than that of control group, and the apoptosis rate of PH group was higher than that of PA and PO group. The difference was statistically significant (P < 0.05).) the level of Ros in the propofol treated group was higher than that in the control group, and the Ros production level in the PH group was significantly higher than that in the PAPPO-COCH group, and the Ros production level in the PH group was significantly higher than that in the control group (P < 0.05), and the Ros production level in the PH group was significantly higher than that in the control group. Compared with PA and PO groups, the expression of SOD in P0.05 + PH group was significantly higher than that in PA and PO group. Conclusion this study preliminarily confirmed that propofol could induce neuron-like PC12 cell apoptosis through oxidative stress injury in hypoxic environment. But its concrete mechanism still needs our further research.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R614

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