[1]许多,刘梅,尹琼玉,等.氧化苦参碱对缺血再灌注损伤小鼠原代海马神经元的保护作用及机制研究[J].临床神经外科杂志,2020,17(04):430-433.[doi:DOI:10.3969/j.issn.1672-7770.2020.04.015]
 XU Duo,LIU Mei,YIN Qiong-yu,et al.Research on the protective effect and mechanism of oxymatrine on primary hippocampal neurons of mice after ischemia-reperfusion injury[J].Journal of Clinical Neurosurgery,2020,17(04):430-433.[doi:DOI:10.3969/j.issn.1672-7770.2020.04.015]
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氧化苦参碱对缺血再灌注损伤小鼠原代海马神经元的保护作用及机制研究()
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《临床神经外科杂志》[ISSN:1672-7770/CN:32-1727/R]

卷:
17
期数:
2020年04期
页码:
430-433
栏目:
论著
出版日期:
2020-08-14

文章信息/Info

Title:
Research on the protective effect and mechanism of oxymatrine on primary hippocampal neurons of mice after ischemia-reperfusion injury
文章编号:
202004015
作者:
许多刘梅尹琼玉周燕萍侯任婕鲁毅杨波
210002 南京,解放军东部战区空军医院药学部
Author(s):
XU Duo LIU Mei YIN Qiong-yu et al.
Department of Pharmacy, Air Force Hospital of Eastern Theater Command, Nanjing 210002, China
关键词:
氧化苦参碱缺血再灌注损伤小鼠原代海马神经元细胞内钙离子浓度L型钙通道Cav1.2
Keywords:
oxymatrine ischemia reperfusion injury mice primary hippocampal neurons intracellular calcium concentration L-type calcium channel Cav1.2
分类号:
R285.5
DOI:
DOI:10.3969/j.issn.1672-7770.2020.04.015
文献标志码:
A
摘要:
目的探讨氧化苦参碱对缺血再灌注损伤海马神经元的保护作用及其机制。方法将小鼠原代海马神经元分为正常对照组、缺血再灌注组和氧化苦参碱组。正常对照组海马神经元予以常规培养;缺血再灌注组海马神经元用氧葡萄糖剥夺/再恢复培养模拟缺血再灌注损伤;氧化苦参碱组海马神经元在氧葡萄糖剥夺后再恢复前,予以200 μg/mL氧化苦参碱。采用流式细胞仪检测各组海马神经元内的游离钙离子浓度;用Western blot法检测各组海马神经元的Cav1.2蛋白表达水平;用膜片钳技术检测各组海马神经元的L型钙通道(L-type calcium channel,LTCC)功能。结果与缺血再灌注组相比,氧化苦参碱组海马神经元的游离钙离子浓度、Cav1.2蛋白表达量及LTCC功能均明显降低(均P<0.05);但仍未恢复到正常对照组水平(均P<0.05)。结论氧化苦参碱可能通过减少小鼠原代海马神经元的Cav1.2表达和LTCC功能,降低细胞内游离钙离子的浓度,从而发挥对缺血再灌注损伤神经元的保护作用。
Abstract:
To investigate the protective effect and mechanism of oxymatrine on primary hippocampal neurons of mice after ischemia-reperfusion injury. Methods The mice primary hippocampal neurons were randomly divided into control group, ischemia reperfusion group and oxymatrine group. The neurons in the control group were cultured in the conventional incubator. The neurons in ischemia reperfusion group were cultured by oxygen-glucose deprivation(OGD)/reperfusion(OGDR) method to simulate ischemia reperfusion injury. The neurons in the oxymatrine group were treated with 200 μg/mL oxymatrine after incubation in hypoxic incubator and before incubation in conventional incubator. After exposure to 20 μM oxymatrine, the intracellular calcium concentration of mice primary hippocampal neurons were tested by flow cytometry. The expression of Cav1.2 was measured by the western blot. The function of L-type calcium channel(LTCC) was measured by patch clamp. Results Compared with the ischemia reperfusion group, exposure to oxymatrine decreased the intracellular calcium concentration of mice primary hippocampal neurons, the expression of Cav1.2 and the function of L-type calcium channel(P<0.05). But all the indexes tested above did not return to the level of control group(P<0.05). Conclusions Oxymatrine may decreases the intracellular calcium concentration of mice primary hippocampal neurons by inhibiting the expression of Cav1.2 and the function of L-type calcium channel. Oxymatrine may play a protective role in neurons after ischemia-reperfusion injury by reducing Cav1.2 expression and the function of L-type voltage-dependent calcium channel in primary hippocampal neurons of mice.
更新日期/Last Update: 2020-08-18