首页|纳洛酮对缺氧诱导大鼠神经元损伤的抑制作用及其机制

纳洛酮对缺氧诱导大鼠神经元损伤的抑制作用及其机制

Study on naloxone blocked hypoxia-induced rat neuron injury

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目的 探讨纳洛酮对缺氧诱导大鼠神经元损伤的作用及其可能的机制.方法 体外培养大鼠神经元,将其分为正常对照组、缺氧诱导组、缺氧诱导+纳洛酮干预组.应用流式细胞术测定大鼠神经元损伤;应用荧光探针2,7-二氯二氢荧光素乙酰乙酸(DCFDA)检测细胞内活性氧的变化;应用比色法检测超氧化物歧化酶(SOD)的活性;应用Western blot检测NF-κB的活化.结果 (1)纳洛酮抑制缺氧诱导的大鼠神经元凋亡,缺氧组大鼠神经元细胞凋亡明显增加,为对照组的3.54倍,纳洛酮干预组为对照组的1.35倍(均P<0.05).(2)纳洛酮抑制缺氧诱导的活性氧生成,缺氧诱导大鼠神经元活性氧生成,为对照组的2.66倍,纳洛酮干预组为对照组的1.24倍(均P<0.05).(3)纳洛酮抑制缺氧诱导的NF-κB活化(P<0.05).(4)抗氧化剂NAC抑制缺氧诱导的NF-κB活化,抑制率达49% (P <0.05).结论 纳洛酮抑制缺氧诱导的活性氧生成,进而抑制NF-κB活化,从而抑制缺氧诱导的大鼠神经元凋亡.
Objective To investigate the effects of naloxone on hypoxia-induced rat neuron injury. Methods Rat neuron were cultured and divided into control group, hypoxia-induced group, naloxone pretreated group. Neuron apoptosis was detected by using flow cytometry. Fluorescent probe, 2,7-dichloro-fluorescein diacetate ( DCFDA) , was used to examine intracellular reactive oxygen species ( ROS) generation. Superoxide dismutase ( SOD) activity was accessed spectrophotometrically by using SOD assay kit. NF-κB activation was detected by western blotting. Results (1 ) Naloxone inhibited hypoxia-induced rat neuron apoptosis. Hypoxic rats neuronal apoptosis significantly increased 3.54 times than that of the control group (all P <0. 05) . (2) Naloxone inhibited hypoxia-induced ROS generation. Hypoxia-induced neuron reactive oxygen species generation, was 2. 66 times than that of the control group, the naloxone pretreatment group was 1. 24 times than that of the control group (all P < 0. 05 ) . (3) Naloxone inhibited hypoxia-induced NF-κB activation(P <0. 05). (4) The antioxidant, NAC, inhibited hypoxia-induced NF-κB activation with inhibition rate of 49% (P <0. 05). Conclusion Naloxone can prevent hypoxia-induced rat neuronal apoptosis by inhibiting hypoxia-induced ROS generation in rat neuron and further blocking NF-κB activation.

hypoxianaloxonerat neuron injuryROS

程真梅、陆卫红、吉山宝、沈南平

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无锡市人民医院儿童重症监护室,江苏无锡214023

缺氧 纳洛酮 大鼠神经元 活性氧

2012

苏州大学学报(医学版)
苏州大学

苏州大学学报(医学版)

CSTPCD
影响因子:0.499
ISSN:1673-0399
年,卷(期):2012.32(6)
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