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白果内酯在PC12细胞中对NO诱导的细胞毒性的保护作用(英文)
引用本文:Song W,Guan HJ,Zhu XZ,Chen ZL,Yin ML,Cheng XF. 白果内酯在PC12细胞中对NO诱导的细胞毒性的保护作用(英文)[J]. Acta pharmacologica Sinica, 2000, 21(5): 415-420
作者姓名:Song W  Guan HJ  Zhu XZ  Chen ZL  Yin ML  Cheng XF
作者单位:中国科学院上海药物研究所,中国科学院上海药物研究所,中国科学院上海药物研究所,中国科学院上海药物研究所,中国科学院上海药物研究所,中国科学院上海药物研究所 上海 200031 中国,上海 200031 中国,上海 200031 中国,上海 200031 中国,上海 200031 中国,上海 200031 中国
基金项目:Project supported by grants from Chinese Minstry of Science and Technology (G1998051108),Shanghai Science and Technology Commission (97XD14018).
摘    要:目的:研究白果内酯在PC12细胞中对NO诱导的细胞毒性的保护作用。方法:以MTT法及LDH法检测细胞存活率;同时检测细胞的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性及脂质过氧化水平。结果:NO供体SIN-1(50-300μmol·L~(-1))可导致PC12细胞死亡,可使PC12细胞脂质过氧化水平升高。白果内酯预孵育可减少NO诱导的细胞死亡;可抑制脂质过氧化水平升高。白果内酯预孵育本身可使SOD及CAT酶活性升高。结论:白果内酯对NO诱导的细胞毒性作用具保护作用,该保护作用可能与白果内酯升高细胞内SOD和CAT的活性有关。

关 键 词:PC12细胞  SIN-1  神经毒素  神经元  细胞存活  脂质过氧化作用  神经保护剂  抗氧化剂  白果内酯

Protective effect of bilobalide against nitric oxide-induced neurotoxicity in PC12 cells
Song W,Guan H J,Zhu X Z,Chen Z L,Yin M L,Cheng X F. Protective effect of bilobalide against nitric oxide-induced neurotoxicity in PC12 cells[J]. Acta pharmacologica Sinica, 2000, 21(5): 415-420
Authors:Song W  Guan H J  Zhu X Z  Chen Z L  Yin M L  Cheng X F
Affiliation:Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 200031, China.
Abstract:AIM: To examine the effects of bilobalide on nitric oxide-induced neurotoxicity in pheochromocytoma-derived PC12 cells (PC12 cells). METHODS: PC12 cell survival was monitored by LDH release and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays. Superoxide dismutases (SOD) and catalase (CAT) activities were measured based on their abilities to inhibit the oxidation of epinephrine by the xanthine-xanthine oxidase system or to decompose H2O2 respectively. The content of malondialdehyde (MDA) was measured by a fluorometric assay to indicate the lipid peroxidation. RESULTS: 3-Morpholinosydnonimine (SIN-1, 50-300 mumol.L-1) induced PC12 cell damage. After the cells had been pretreated with 10 mumol.L-1 bilobalide for 24 h, the cell viability was increased to 91% +/- 30% from 52% +/- 14% in SIN-1 alone group. Moreover, the activities of SOD and CAT were increased after cells were treated with bilobalide. CONCLUSION: The NO-induced neurotoxicity can be protected by bilobalide in PC12 cells. The bilobalide-induced increase in SOD and CAT activities may serve as one of the mechanisms underlying the neuroprotective effect of bilobalide.
Keywords:PC12 cells  SIN-1  neurotoxins  neurons  cell survival  lipid peroxidation  neuroprotective agents  antioxidants  bilobalide
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