期刊文献+

梓醇对鱼藤酮所致小鼠脑线粒体损伤的保护作用 被引量:4

Protective Effect of Catalpol Against Mice Brain Mitochondrial Injuries Induced by Rotenone
原文传递
导出
摘要 目的:研究梓醇对鱼藤酮所致小鼠脑线粒体损伤的保护作用。方法:小鼠随机分为对照组、模型组和治疗组。模型组腹腔注射鱼藤酮21d;治疗组先注射鱼藤酮21 d,后用梓醇治疗10 d。测定小鼠中脑、纹状体和皮层中线粒体复合酶Ⅰ、谷胱甘肽(GSH)、乳酸脱氢酶(LDH)活性、膜电位、活性氧(ROS)的含量。结果:梓醇能够提高小鼠复合酶Ⅰ活性,增加GSH的含量,减少膜电位的丢失和活性氧的生成,抑制LDH的释放。结论:梓醇对鱼藤酮损伤小鼠脑线粒体具有保护作用。 ABSTRACT Objective: To study the effect of catalpol on the mitochondrial function of mice brain mitochondrial on rotenone-induced damage in mice. Methods: Mice were randomly divided into three group, control group, model group and therapy group. Model group was injected intraperitoneally (i.p.) with rotenone (1.5 mg/kg) for 21 days, therapy group was injected with rotenone for 21 days, then given catalpol (10 mg/kg) for 10 days. The activities of complex I and lactic dehydrogenase (LDH), mitochondrial membrane potential, content of reduced glutathione (GSH) and reactive oxygen species (ROS) in midbrain, striatum and cortex mitochondria of mice were assayed. Results: Catalpol could increase the activities of complex I, increase GSH contents, decrease the loss of mitochondrial membrane potential and restrain the release of LDH. Conclusion: Catalpol has protective effect on mice brain mitochondrial injury induced by rotenone. Key words: Catalpol; Rotenone; Mice; Mitochondria
出处 《现代生物医学进展》 CAS 2012年第29期5661-5664,共4页 Progress in Modern Biomedicine
基金 科技部国际科技合作重点项目计划(No.2005DFA40790)
关键词 梓醇 鱼藤酮 小鼠 线粒体 Catalpol Rotenone Mice Mitochondria
  • 相关文献

参考文献20

  • 1Vemice Jackson-Lewis, Javier Blesa, Serge PrzedborskiAnimal mod- els of Parkinson's disease [J]. Parkinsonism & Related Disorders, 2012, 18(Supplement 1): S183-S185.
  • 2Mulcahy, P. Walsh S. Paucard A,. Characterisation of a novel model of Parkinson's disease by intra-striatal infusion of the pesticide rotenone[J]. Neuroscience, 2011, 181 (5): 234-242.
  • 3Bi J, Jiang B, Hao S, Zhang A, Dong Y, Jiang T, An LJ. Catalpol at- tenuates nitric oxide increase via ERK signaling pathways induced by rotenone in mesencephalic neurons[J]. Neurochemistry International, 2009, 54:264-270.
  • 4Jiang B, Du J, Bao YM, An LJ. Catalpol attenuates the neurotoxicity induced by 13-Amyloidl-42 in cortical neuron-glia cultures [J]. Brain Research, 2008, 1188:139-147.
  • 5Jiang B, Zhang H, Bing J, et al. Neuroprotective activities of catalpol on MPP+/MPTP-induced neurotoxicity [J]. Neurological Research, 2008, 30(6): 639-644.
  • 6Zhang A, Hao S, Bi J, et al. Effects of catalpol on mitochondrial func- tion and working memory in mice after LPS-induced acute systemic inflammation [J]. Experimental and Toxicologic pathology, 2009, (5) 61:461-469.
  • 7Veitch K, Hombroeckx A, Caucheteux D, et al. Global ischemia in- duces a biphasic response of the mitochondrial respiratory chain. Anoxic pre-perfusion protects against ischemic damage [J]. Biochem J, 1992, 281(Pt 3): 709-715.
  • 8Kushnareva Y, Murphy AN, Andreyev A, et al. Complex I-mediated reactive oxygen species generation: modulation by cytochrome c and NAD (P)+ oxidation- reduction state [J]. Biochem J, 2002, 368(2): 545-553.
  • 9Emaus RK, Grunwald R, Lemasters JJ, et al. Rhodamin 123 as a probe oftransmembrane potential in isolated rat-liver mitochondria: spectral and metabolic properties [J]. Biochim Biophys Acta, 1986, 850(3): 436-448.
  • 10Hamai D, Campbell A, Bondy SC, et al. Modulation of oxidative events by multivalent manganese complexes in brain tissue [J]. Free Rad Biol Med, 2001, 31 (6): 763-768.

同被引文献48

引证文献4

二级引证文献247

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部