摘要
目的观察川芎嗪烟酸酯(TMPN)对H2O2引起的体外培养大鼠脑皮层神经细胞及人神经母细胞瘤细胞(SH-SY5Y)氧化性损伤的保护作用,并初步探讨其作用机制。方法H2O2诱导体外培养大鼠脑皮层神经元及SH-SY5Y细胞进入氧化应激状态,观察TMPN对神经细胞氧化损伤的保护作用。结果TMPN能显著升高氧化损伤神经细胞的存活率,减少乳酸脱氢酶(LDH)的漏出,对H2O2诱导的神经细胞内游离钙浓度([Ca2+]I)的升高有明显的抑制作用,并能减少胞内脂质过氧化物丙二醛(MDA)的生成,提高谷胱甘肽过氧物酶(GSH-Px)含量及超氧化物歧化酶(SOD)活性。结论TMPN可以有效保护活性氧对培养大鼠脑皮层神经元及SH-SY5Y细胞的氧化损伤,维持细胞的正常生理功能,其机制可能与TMPN抑制H2O2诱导的[Ca2+]I异常升高,减少脂质过氧化物生成,增加抗氧化物质的含量有关。
Abstract
OBJECTIVE To investigate the protection of tetramethylpyrazine nicolate on oxidative damage in both primary cortical cells and human neuroblastoma cells line(SH-SY5Y).METHODS Both primary cortical cells and human neuroblastoma SH-SY5Y cells line were injured using H2O2.The protective effect of tetramethylpyrazine nicolate on nerve cells was observed.RESULTS TMPN increased the injured cells surrival rate,decreased partly the leak of lactate dehydrogenase(LDH).TMPN reduced the elevated level of intracellular calcium concentration([Ca2+]i)and malondialdehyde(MDA) induced by oxidative damage,increased the activity of superoxide dismutase(SOD) and the contents of Glutathione peroxidase(GSH-Px) level in injuried cells.CONCLUSION TMPN has potent protection on oxidative damage,its potential mechanism relates to suppressing the generation of reactive oxygen species and inhibiting the intra-cellular calcium overload.
关键词
川芎嗪烟酸酯 /
神经细胞 /
氧化损伤
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Key words
tetramethylpyrazine nicolate /
nerve cell /
oxidative damage
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赵丽霞;郭秀丽;刘新泳.
川芎嗪烟酸酯对神经细胞氧化损伤的保护作用[J]. 中国药学杂志, 2006, 41(06): 420-423
ZHO Li-xi;GUO Xiu-li;LIU Xin-yong.
Protective Effect of Tetramethylpyrazine Nicolate on Nerve Cells Injured by Hydrogen Peroxide [J]. Chinese Pharmaceutical Journal, 2006, 41(06): 420-423
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脚注
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基金
山东省卫生系统高层次人才1020工程项目;济南市青年科技明星计划资助课题
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