原儿茶酸对帕金森模型鼠脑组织抗氧化能力的影响

被引：22

作者：

张秀丽 ^{[1
]}

李亚晨 ^{[2
]}

牛新华 ^{[1
]}

张树平 ^{[1
]}

机构：

[1] 滨州医学院

[2] 大连医科大学

来源：

现代生物医学进展 | 2011年 / 11卷 / 17期

关键词：

原儿茶酸; 帕金森; 鱼藤酮; 抗氧化作用; 神经保护;

D O I：

10.13241/j.cnki.pmb.2011.17.012

中图分类号：

R285.5 [中药实验药理];

学科分类号：

摘要：

目的:观察原儿茶酸对鱼藤酮诱导的帕金森模型小鼠脑组织中相关抗氧化酶活性的影响,为原儿茶酸治疗帕金森病提供理论依据。方法:选用昆明小鼠为实验动物,连续5周腹腔注射鱼藤酮(1mg/kg.d)建立帕金森模型,之后2周分别注射原儿茶酸(5mg/kg.d)和阳性药物美多芭(125mg/kg.d)。应用生物化学方法,观察原儿茶酸对帕金森模型小鼠中脑和纹状体内超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)活力以及脂质过氧化物丙二醛(MDA)含量的影响。结果:实验数据显示原儿茶酸可提高帕金森模型小鼠中脑和纹状体SOD、CAT、GSH-PX活力,降低MDA含量。同时病理切片染色显示原儿茶酸可减轻鱼藤酮诱导的脑组织损伤。结论:原儿茶酸具有神经保护作用,保护机制可能是提高脑组织内源性抗氧化酶活力,减少体内自由基的产生,进而减轻了脑组织的病理损伤。

引用

页码：3248 / 3251

页数：4

共 19 条

[1] Protective effect of protocatechuic acid from Alpinia oxyphylla on hydrogen peroxide-induced oxidative PC12 cell death[J] . Shui Guan,Yong-Ming Bao,Bo Jiang,Li-Jia An. &nbspEuropean Journal of Pharmacology . 2006 (1)
[2] Dose response of alcohol-induced changes in BP, nitric oxide and antioxidants in rat plasma. Husain K,Mejia J,Lalla J, et al. Pharmacological Research . 2005
[3] Protocatechuic acid suppresses MPP+-induced mitochondrial dysfunction and apoptotic cell death in PC12 cells
Guan, S.
Jiang, B.
Bao, Y. M.
An, L. J.
[J]. FOOD AND CHEMICAL TOXICOLOGY, 2006, 44 (10) : 1659 - 1666
[4] Parkinson’s Disease: Current and Future Challenges[J] . J.William Langston. &nbspNeurotoxicology . 2002 (4)
[5] 重复注射鱼藤酮对中枢多巴胺神经元的毒性作用
李云鹏
董兆君
王仕丽
蔡颖
李奇慧
乐卫东
[J]. 第三军医大学学报, 2003, (13) : 1123 - 1126
[6] The relevance of malondialdehyde as a biochemical index of lipid peroxidation of postischemic tissues in the rat and human beings[J] . G. Lazzarino,B. Tavazzi,D. Pierro,R. Vagnozzi,M. Penco,B. Giardina. &nbspBiological Trace Element Research . 1995 (1)
[7] Protocatechuic acid suppresses MPP+-induced mitochondrial dysfunction and apoptotic cell death in PC12cells. Guan S,Jiang B,Bao YM,et al. Food and Chemical Toxicology . 2006
[8] Thiol redox state and oxidative stress in midbrain and striatum of weaver mutant mice,a genetic model of nigrostriatal dopamine deficiency. Nikolaos P,Ioannis P,George Z,et al. Neuroscience Letters . 2005
[9] Subcutaneous rotenone exposure causes highly selective dopaminergic degeneration and alpha-synuclein aggregation. Sherer TB, Kim JH, Betarbet R, et al. Experimental Neurology . 2003
[10] Biomarkersof cell damage induced by oxidative stress in Parkinson’’s disease andrelated models. Tobón-Velasco JC,Carmona-Aparicio L,Ali SF,et al. Cent Nerv Syst Agents Med Chem . 2010

← 1 2 →