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黄芪多糖对星形胶质细胞培养液中自由基系统损伤保护作用的时间依赖性 被引量:8

Time dependency of astragalus polysaccharides against systemic injury of free radical in astrocyte culture medium
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摘要 目的:观察具有抗炎、调节免疫、延缓神经元变性等药理作用的黄芪多糖对胶质细胞培养液中谷胱甘肽和丙二醛含量及谷胱甘肽过氧化物酶的活性、超氧化物歧化酶活力的影响,探讨黄芪多糖对左旋多巴致胶质细胞培养液中自由基系统动态平衡损害的保护作用,分析该种作用与时间的关系。方法:实验于2003-12/2004-9在泰山医学院基础研究所完成。①选用出生2d的SD大鼠10只,雌雄不拘。②按照McCarthy和deVelli的方法进行星形胶质细胞的原代培养,胶质细胞培养液建立左旋多巴损伤模型,实验分为3组(每6孔细胞液一组):正常对照组(正常细胞培养,加入等数量的培养基,不加任何药物),左旋多巴组(加入100μmol/L左旋多巴),黄芪多糖+左旋多巴[加入黄芪多糖(由合肥恒星药物研究所提供)20mg/L和左旋多巴100μmol/L]。分别在培养4,24,48和72h后取处理后的含胶质细胞培养液。③采用比色定量法测谷胱甘肽含量,比色法测谷胱甘肽过氧化物酶活性,黄嘌呤氧化酶法测超氧化物歧化酶活力,硫代巴比妥酸法测定丙二醛含量。④计量资料差异比较采用方差分析。结果:①谷胱甘肽含量及谷胱甘肽过氧化物酶、超氧化物歧化酶活力:培养4h后各组差异不明显。培养24,48和72h后,左旋多巴组明显低于空白对照组(P<0.05~0.01);黄芪多糖+左旋多巴组低于空白对照组,但差异不明显(P>0.05),明显高于左旋多巴组(P<0.05)。②丙二醛含量:培养4h后各组差异不明显。培养24,48和72h后,左旋多巴组明显高于空白对照组(P<0.05~0.01);黄芪多糖+左旋多巴组高于空白对照组,但差异不明显(P>0.05),明显低于左旋多巴组(P<0.05)。结论:左旋多巴自身氧化产生大量的自由基,促进帕金森病发展,黄芪多糖可降低左旋多巴对神经元的毒性作用,作用有时间依赖性。 AIM: To investigate the effect of astragalus polysaccharides (APS) characterized by anti-inflammation, adjusting immune and delaying neuronal degeaeration on contents of estathion and malondialdehyde (MDA), activities of glutathione peroxidase and superoxide dismutase (SOD) in astrocyte culture medium, and to discuss proteetive effect of APS on dynamic equilibrium injury of free radical system in hendopa-indueed astroeyte culture medium so as to analyze the relationship with time. METHODS: The experiment was completed in the Basic Research hlstitute of Taishan Medical College from December 2003 to September 2004. ① Ten postnatal newborn SD rats, with 2-day old, of either gender, were selected.② Primary culture of astrocyte was performed with McCarthy and deVelli methods, and astroeyte culture medium was used to establish injured model of bendopa. Rats were divided into 3 groups (6- well medium ill each group): normal control group (normal cellular culture, the same volume of culture mediunl, without any drug), bendopa group (100μmol/L bendopa) and APS + bendopa group [20 mg/L APS (provided by Hefei Hengxing Pharmaceutical Institute) and 100 μmol/Lbendopa]. Culture medium was dealt with after 4, 24, 48 anti 72 hours after culture respectively. ③ Content of estathion was assayed with colorimetric quantity technique: activity of glutathione peroxidase with chromatometry; SOD activity with xanthine oxidase method; and MDA content with thiolharbituric acid method,④ Measurement data were compared with analysis of variance. RESULTS: ① Content of estathion and activities of glutathione peroxidase and SOD: There was not significant difference after 4-hour culture..Values in bendopa group were lower than those in blank control group 24, 48 and 72 hours after culture (P 〈 0.05-0.01 ); and those in APS + bendopa group were lower than those in blank control group with insignificant difference (P 〉 0.05), but were higher than those in bendopa group (P 〈 0.05). ② MDA content: There was not significant difference after 4-hour cuhure. Contents in bendopa group were higher than those in hlank control group 24, 48 and 72 hours after culture (P 〈 0.05-0.01); and those iu APS + bendopa group were higher than those in blank control group with insignificant difference (P 〉 0.05), but were lower than those in bendopa group (P 〈 0.05). CONCLUSION: Free radical produced by self-oxidation of bendopa can promote development of Parkinson disease. APS can relieve the toxicity of bendopa on neurons and the effect has time dependency,
出处 《中国临床康复》 CAS CSCD 北大核心 2006年第11期59-61,共3页 Chinese Journal of Clinical Rehabilitation
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参考文献11

  • 1Zhang ZX,Roman GC.Worldwide occurrence of Parkinson's disease:an updated review.Neuroepidemiology 1993;12(4):195-208.
  • 2Kostrzewa RM,Kostrzewa JP,Brus R.Neuroprotective and neurotoxic role of levodopa (L-DOPA) in neurodegenerative disorders relating to Parkinson's disease.Amino Acids 2002;23:57-63.
  • 3McCarthy KD,de Vellis J.Preparation of separate astroglial and oligodendroglial cell cultures from rat cerebral tissue.J Cell Biol 1980;85(3):890-902.
  • 4曹非,孙圣刚,陈吉相,童萼塘,张敏.帕金森病大鼠黑质细胞凋亡与左旋多巴剂量的关系(英文)[J].中国临床康复,2003,7(22):3052-3053. 被引量:8
  • 5Heales SJ,Lam AA,Duncan AJ,et al.Neurodegeneration or neuroprotection:the pivotal role of astrocytes.Neurochem Res 2004;29(3):513-9.
  • 6Melamed E,Offen D,Shirvan A,et al.Levodopa toxicity and apoptosis.Ann Neurol 1998;44(3 Suppl 1):S149-54.
  • 7Mytilineou C,Walker RH,Jnobaptiste R,et al.Levodopa is toxic to dopamine neurons in an in vitro but not an in vivo model of oxidative stress.J Pharmacol Exp Ther 2003;304(2):792-800.
  • 8Romero FJ,Bosch-Morell F,Romero MJ,et al.Lipid peroxidation products and antioxidants in human disease.Environ Health Perspect 1998;106 Suppl 5:1229-34.
  • 9Soliman MK,Mazzio E,Soliman KF.Levodopa modulating effects of inducible nitric oxide synthase and reactive oxygen species in glioma cells.Life Sci 2002;72(2):185-98.
  • 10Loeffler DA,Lewitt PA,Juneau PL,et al.Time-dependent effects of Levodopa on regional brain dopamine metabolism and lipid peroxidation.Brain Res Bull 1998;47(6):663-7.

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