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低氧環(huán)境下丙泊酚致PC12細胞損傷的機制研究

發(fā)布時間:2018-03-11 20:54

  本文選題:丙泊酚 切入點:低氧 出處:《重慶醫(yī)科大學(xué)》2017年碩士論文 論文類型:學(xué)位論文


【摘要】:目的丙泊酚是臨床麻醉最常用的靜脈麻醉藥之一,丙泊酚的反復(fù)應(yīng)用可引起神經(jīng)細胞凋亡增加,損傷學(xué)習(xí)、記憶、認知功能,低氧是圍手術(shù)期容易被忽略的并發(fā)癥,也是引起細胞凋亡、認知功能障礙的重要因素之一。本研究以神經(jīng)元樣PC12細胞為研究對象,從氧化應(yīng)激角度對低氧環(huán)境下丙泊酚對PC12細胞株凋亡的影響及機制進行探討,為有效干預(yù)麻醉手術(shù)后并發(fā)癥的發(fā)生及術(shù)后認知功能障礙的治療提供新的思路。方法將PC12細胞接種于培養(yǎng)板中,采用隨機數(shù)字表法,將其隨機分為6組:丙泊酚低氧組(PH組)、丙泊酚空氣組(PA組)和丙泊酚氧氣組(PO組),丙泊酚濃度為10μM。低氧對照組(CH組)、空氣對照組(CA組)和氧氣對照組(CO組)。藥物處理完畢后分別放入低氧(5%O2),空氣和氧氣(35%O2)環(huán)境的細胞培養(yǎng)箱培養(yǎng),8小時后進行流式檢測細胞凋亡情況,檢測細胞內(nèi)ROS水平和細胞SOD酶活力。結(jié)果(1)MTT分析發(fā)現(xiàn),丙泊酚10μM干預(yù)8h對PC12細胞的增殖有明顯抑制作用(P0.05)。(2)丙泊酚處理組凋亡率均大于各對照組,且PH組凋亡率大于PA及PO組,差異具有統(tǒng)計學(xué)意義(P0.05)。(3)各丙泊酚處理組PA、PO、PH組,較各對照組CA、CO、CH組,ROS水平均有升高;并且PH組較PA、PO組,ROS生成水平明顯升高。(4)與CA、CO、CH組相比,各PA、PO、PH中SOD表達明顯增加(P0.05),PH組SOD水平較PA及PO組顯著增加(P0.05)。結(jié)論本研究初步證實低氧環(huán)境下丙泊酚可通過氧化應(yīng)激損傷導(dǎo)致神經(jīng)元樣PC12細胞凋亡增加,但其具體機制仍需我們進一步的研究。
[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.
【學(xué)位授予單位】:重慶醫(yī)科大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2017
【分類號】:R614

【參考文獻】

相關(guān)期刊論文 前1條

1 于布為,薛慶生,夏夢,王澤劍,陳紅專;丙泊酚對大鼠腦片不同性質(zhì)損傷的影響[J];中華醫(yī)學(xué)雜志;2003年13期



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