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去卵巢大鼠脑内凋亡基因蛋白表达及半枝莲黄酮的干预作用 被引量:6

Effect of flavonoids from Scutellaria barbata on protein expression of apoptotic genes in the brain of ovariectomized rats
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摘要 目的:探讨去卵巢大鼠脑内凋亡基因Bcl-2,Bax和p53的蛋白表达及半枝莲黄酮(Scutellaria barbata flavonoid,SBF)的干预作用。方法:摘除3月龄雌性Sprague-dawley(SD)大鼠卵巢10个月,模拟老年性痴呆(Alzheimer's disease,AD)模型,采用免疫组化法检测脑内凋亡基因Bcl-2,Bax和p53的蛋白表达,评价SBF对摘除卵巢诱导大鼠神经细胞凋亡的抑制作用。结果:摘除大鼠双侧卵巢可使大脑皮质中Bcl-2,Bax和p53的表达异常改变,Bcl-2阳性表达神经元数量明显减少,Bax和p53阳性表达神经元数量明显增多。去卵巢大鼠连续36 d灌胃(ig)SBF17.5,35和70 mg.kg-1可不同程度地改善去卵巢大鼠大脑皮层凋亡基因的异常表达。结论:摘除大鼠卵巢10个月可以诱导神经细胞凋亡,SBF对神经细胞凋亡有对抗作用,提示SBF可能有利于对AD的治疗。 Objective: To study the protein expression of apoptotic genes in the brain of ovariectomized rats and the effect of flavonoids from Scutellaria barbata(SBF).Methods: Sprague-Dawley(SD) female rats(3 months old) were ovariectomized for 10 months to mimic AD-like disorder.The effect of SBF on neuron apoptosis in ovarietomized rats were evaluated by detecting protein expression of Bcl-2,Bax and p53 with immunohistochemical methods.Results: Ovarietomized rats exhibited abnormal changes in the protein expression of Bcl-2,Bax and p53 genes.Bcl-2 positive neurons were significantly increased,and Bax and p53 positive neurons were markedly decreased in ovarietomized rats.These abnormal changes in ovarietomized rats were attenuated by daily administrated SBF 17.5,35 and 70 mg·kg^-1 for consecutive 36 days.Conclusion: The ovariectomy can result in neuron apoptosis after 10 months in rats,and this apoptosis can be inhibited by SBF treatment for 36 days,suggesting that SBF may be beneficial to AD.
出处 《中国新药杂志》 CAS CSCD 北大核心 2010年第14期1255-1259,共5页 Chinese Journal of New Drugs
基金 河北省自然基金(C2009001007) 河北省中医药管理局资助项目(05027)
关键词 半枝莲黄酮 去卵巢大鼠 BCL-2 BAX P53 免疫组化 Scutellaria barbata flavonoids ovariectomized rats Bcl-2 Bax p53 immunohistochemistry
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  • 1刘英华,尹君,王丹玲,王建枝.载脂蛋白E与阿尔茨海默病的关系[J].生命的化学,2005,25(1):10-12. 被引量:10
  • 2贾晓静,贾少杰,张昱,李晶.雌激素、apoE与阿尔茨海默病[J].中国老年学杂志,2007,27(6):593-596. 被引量:5
  • 3杨硕,翟东旭,王广友,徐望舒,赵然,李国忠,金连弘,李呼伦.晚期糖基化终产物受体在脑缺血损伤中的表达及作用机制[J].中风与神经疾病杂志,2007,24(2):169-172. 被引量:4
  • 4曾芳,余曙光,唐勇,邵欣.老年性痴呆复合动物模型研究概况(综述)[J].中国神经免疫学和神经病学杂志,2007,14(4):197-200. 被引量:14
  • 5马永兴,俞卓伟.现代痴呆学[M].第1版.北京:科学技术文献出版社,2007:295-302.
  • 6Evans JC,Wisen S,Gestwicki JE. Heat shock proteins 70 and90 inhibit early stages of amyloid beta-( 1-42) aggregation invitroU].} Biol Chem,2006,281(44) ;33182-33191.
  • 7Ltith HJ,Holzer M,Gartner U,et al. Expression of endothe-lial and inducible NOS-isoforms is increased in Alzheimer,sdisease, in APP23 transgenic mice and after experimentalbrain lesion in rat: evidence for an induction by amyloidpathology[ J]. Brain Res,2001,913( 1) :57-67.
  • 8Fonte V,Kapulkin V,Taft A,et al. Interaction of intracel-lular beta amyloid peptide with chaperone proteins [ J].Proc Natl Acad Sci U S A,2002,99( 14) :9439-9444.
  • 9Kakimura J,Kitamura Y,Takata K,et al. Microglial activa-tion and amyloid-beta clearance induced by exogenousheat-shock proteins[ J]. FASEB J,2002,16(6) :601-603.
  • 10Schmechel DE, Saunders AM, Strittmatter WJ, et al. In-creased amyloid beta-peptide deposition in cerebral cortexas a consequence of apolipoprotein E genotype in late-onsetAlzheimer disease[ J]. Proc Natl Acad Sci U S A, 1993 ,90(20):9649-9653.

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