期刊文献+

维生素B_5对全饥饿大鼠脑组织脂质过氧化的动态变化及保护作用 被引量:1

The protective effect of vitamin B_5 on lipid peroxidation in starved rats′brain
在线阅读 下载PDF
导出
摘要 目的观察维生素B5(泛酸)对全饥饿大鼠脑脂质过氧化产物丙二醛(MDA)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)的动态变化及保护作用。方法以饥饿昆明大鼠为模型,灌胃补充维生素B5,观察大鼠饥饿后不同时期脑MDA、GSH、GSH-Px及SOD的变化。结果饥饿后大鼠脑MDA含量明显升高,补充维生素B5后大鼠脑组织MDA含量在禁食4d与7d较饥饿前无明显升高,与全饥饿对照组比较差异有统计学意义。维生素B5对饥饿大鼠脑SOD,GSH-Px活力无影响,但显著提高GSH水平。结论维生素B5能减轻饥饿对大鼠脑组织氧化应激反应。 Objective To study the effect of vitamin Bs on lipid peroxidation in starved rats' brain. Methods To inject vitamin Bs intragastricly to starved rats, then to examine brain MDA, GSH content and the activity of GSH-Px and SOD at different fasting period. Results The level of MDA was significantly increased in rat's brain after starvation. Upon vitamin B5 treatment, there was no obvious increase of MDA between normal rats and rats starved for 5 days or 7 days. However, when compared to the starved group, there was significant decrease after vitamin Bs treatment. Moreover, vitamin Bs had no effect on the activity of SOD and GSH-Px in starved rat's brain, but it could enhance the level of GSH. Conclusion Vitamin Bs can protect rats from harmful lipid peroxida- tion and some of the mechanisms were probably due to enhancing the level of GSH.
出处 《山西医药杂志(上半月)》 CAS 2013年第12期1335-1337,共3页 Shanxi Medical Journal
基金 国家自然科学基金(81370084)
关键词 饥饿 维生素B5 脂质过氧化作用 抗氧化物酶 Hunger Vitamin BS Lipid peroxidation Peroxidase
  • 相关文献

参考文献8

  • 1杨延辉 肖春玲.泛酸的功能和生物合成.生命的化学,2008,28(4):448-452.
  • 2丁玉琴.泛酸在脂肪酸代谢中的作用[J].国外医学(卫生学分册),2000,27(5):304-306. 被引量:14
  • 3印大中.衰老奥秘研究最新进展:自由基氧化-非酶糖基化衰老学说[J].现代中西医结合杂志,2005,14(1):7-10. 被引量:22
  • 4Takayasu Y,Nakaki J, Kawasaki T, et al. Edaravone, a radicalscavenger, inhibits mitochondrial permeability transition porein rat brain. Pharmacol Sci,2007,103 :434-437.
  • 5Rubio V,Zhang JW,Valverde M,et al. Essen-tial role of Nrf2 in protection against hydroquinone and benzo-quinone induced eytotoxieity. Toxicol in Vitro,2011,25(2) : 521-529.
  • 6Dickinson BC, Chang CJ. Chemistry and biology of reactiveoxygen species in signaling or stress responses. Nat ChemBiol,2011,7(8) :504-511.
  • 7Thannickal VJ Fanburg BL. Reactive oxygen species in cellsignaling. Am J Physiol Lung Cell Mol Physiol,2000,279(6):1005-1028.
  • 8Correia SC, Santos RX, Perry G, et al. Mitochondrial impor-tance in Alzheimer's,Huntington-s and Parkinson's diseases.Adv Exp Med Biol,2012,724: 205-221.

二级参考文献20

  • 1Halliwell B, Gutteridge JMC. Free Radical in Biology and Medicine[ M]. 3rd ed. Oxford:Clarendon Press, 1999:1 - 35.
  • 2Esterbauer H, Schaur R J, Zollner H. Chemistry and biochemistry of 4- hydroxy-nonenal, malondialdehyde and related aldehydes[ J ].Free Radic Boil Med, 1991,11(2) :81 - 128.
  • 3Hodge JE. Dehydrated foods, chemistry of browning reactions in model systems[J ]. J Agric Food Chem, 1953,1(15) :928 - 943.
  • 4Baynes JW, Monnier VM. The MaiUard Reaction in Aging, Diabetes and Nutrition[ M]. New York:Alan R Liss, 1989 :
  • 5Monnier VM. Nonenzymatic glycosylation, the Mainard reaction and aging process[J]. Gerontol,1990,45:B105 - 111.
  • 6Brownlee M. Glycosylation products as toxic mediators of diabetic complications[ J ]. Annu Rev Med, 1991,42 : 159 - 166.
  • 7Bucala R, Vlassara H, Cerami A. Advanced glycosylation endproducts:role in diabetic and non-diabetic vascular disease[J]. Drug Dev Res, 1994,32(1) :77 - 89.
  • 8Hipkiss AR,Brownson C,Carrier MJ. Carnosine, the anti-ageing,anti-oxidant dipeptide, may react with protein carbonyl groups[J ].Mech Ageing Dev,2001,122(13) : 1431 - 1445.
  • 9Dukic-Stefanovic S,Schinzel R, Munch G,et al. AGEs in brain ageing:AGE-inhibitors as neuroprotective and anti-dementia drugs[ J ],Biogerontol, 2001,2 ( 1 ) : 19 - 34.
  • 10Orr WC, Sohal RS. Extension of life-span by overexpression of superoxide dismutase and catalase in Drosophila melanogaster [ J ].Science, 1994,263(5150) : 1128 - 1130.

共引文献39

同被引文献4

引证文献1

二级引证文献4

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