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脑脉泰对大鼠脑缺血再灌注后神经细胞凋亡和Akt,bcl-243,Bax和caspase3表达的影响 被引量:5

Effect of Naomaitai on neurocyte apoptosis and the expression of Akt,bcl-2,Bax and caspase3 in rats with cerebral ischemic reperfusion injury
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摘要 目的研究脑脉泰对大鼠脑缺血再灌注损伤神经细胞凋亡和Akt、bcl-2、Bax、caspase3表达的影响。方法采用大鼠大脑中动脉栓塞再灌注动物模型,将雄性SD大鼠随机分为假手术组(sham)、脑缺血再灌注模型组(MCAO)、脑脉泰大剂量组(MCAO+脑脉泰2.24g/kg)、脑脉泰中剂量组(MCAO+脑脉泰1.12g/kg)、脑脉泰小剂量组(MCAO+脑脉泰0.56g/kg),每组10只大鼠。脑脉泰组在MCAO前5天开始灌胃给药,连续5d。用TUNEL法和免疫组化染色法分别检测缺血半暗带凋亡细胞和Akt、bcl-2、Bax和caspase3表达。结果脑脉泰大剂量组和中剂量组大鼠脑缺血半暗带的凋亡细胞显著减少(P<0.01),Akt、bcl-2表达显著增加,caspase3和Bax表达减少,与MCAO模型组比较,有显著性差异(分别为P<0.05和P<0.01)。结论脑脉泰对脑缺血/再灌注损伤有保护作用,其保护作用与促进Akt和bcl-2的表达,抑制Bax和caspasse3的表达有关。 Objective To investigate the effects of Naomaitai on neuron apoptosis and the expression of Akt, bcl-2, Bax and caspase3 in rats with local cerebral ischemic reperfusion. Methods Male Sprague-Dawley rats were randomized into five groups ( n = 10 each) : sham-operated, middle cerebral artery occlusion (MCAO), Naomaitai treatment MCAO (2.24, 1.12 and 0.56 g/kg). Focal cerebral ischemia/reperfusion model was prepaved by transient occlusion of the middle cerebral artery for 90 minutes followed by 24 hrs reperfusion. Naomaitai was administered daily five days before operation. Twenty-four hrs after reperfusion, the brains were obtained for TUNEL staining, and Akt, bcl-2, Bax and caspase3 expression was detected by immunohistochemistry method. Results In the 1.12 g/kg and the 2.24 g/kg Naomaitai treatment groups, the apoptotic cells significantly decreased compared with the MCAO group (P 〈 0.01 ). The protein expression of Bax and caspase3 was lower, while the Akt and bcl-2 protein expression were significantly higher in the Naomaitai treatment groups (1.12 g/kg and 2.24 g/kg) than those in the MCAO group (P 〈0.05, P 〈0. 01 ). Conclusions Naomaitai may have protective effects against cerebral ischemic reperfusion injury, possibly through increasing expression of Akt and bcl-2, and decreasing expression of Bax and caspase3.
出处 《国际神经病学神经外科学杂志》 2009年第4期303-306,共4页 Journal of International Neurology and Neurosurgery
关键词 脑脉泰 脑缺血 细胞凋亡 AKT bcl-2 BAX CASPASE3 Naomaitai Cerebral ischemia-reperfusion Apoptosis Akt Bcl-2 Bax Caspase3
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参考文献12

  • 1Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke, 1989, 20( 1 ) : 84-91.
  • 2Memezawa H, Minamisawa H, Smith ML, et al. Ischemic penumbra in a model of reversible middle cerebral artery occlusion in the rat. Exp Brain Res, 1992, 89( 1 ) : 67-78.
  • 3Ferret I. Apoptosis: Future Targets for Neuroprotective Strategies. Cerebrovasc Dis, 2006, 21 ( Suppl 2) : 9-20.
  • 4Wu CH, Fujihara H, Yao J. Different Expression Patterns of Bcl-2, Bcl-xl, and Bax Proteins After Sublethal Forebrain Ischemia in C57Black/Crj6 Mouse Striatum. Stroke, 2003, 34(7) : 1803-1808.
  • 5Soane L, Fiskum G. Inhibition of Mitochondrial Neural Cell Death Pathways by Protein Transduction of Bcl-2 Family Proteins. J Bioenerg Biomembr. Minireview Series: Mitochondria and Apoptosis, 2005, 37(3) : 179-190.
  • 6Group I. Cerebral Ischemia/Molecular Biology. J Neurosurg Anesthesiol, 2003 , 15 ( 4 ) : 362-364.
  • 7Degterev A, Boyce M, Yuan J. A decade of caspases. Oncogene, 2003, 22(53): 8543-8567.
  • 8陈春美,杨卫忠,王春华,石松生,易海波,陈晓斌,蔡冬生,杨意堃.NOS、p38MAPK、Caspase-3介导大鼠脑缺血神经细胞凋亡可能通路的实验研究[J].国际神经病学神经外科学杂志,2008,35(2):107-111. 被引量:17
  • 9吴建华,谢立新,方芳,方云祥.法舒地尔可能通过PI3-K/Akt信号通路抑制大鼠脑缺血/再灌注区神经元的凋亡[J].中国药理学通报,2008,24(12):1569-1573. 被引量:7
  • 10Dudek H, Datta SR, Frabke TF, et al. Regulation of neuronal survival by the serinethreonine protein kinase Akt. Science, 1997, 275(5300) : 661-665.

二级参考文献21

  • 1邵建林,王玲玲,王俊科,朱俊超,吴滨阳.七氟烷激活PI_3-K/Akt/P^(70S6K)信号转导通路抑制缺血/再灌注损伤神经元的凋亡[J].中国药理学通报,2006,22(11):1362-1366. 被引量:15
  • 2陈春美,杨卫忠,王春华,石松生,蓝佛琳,涂献坤.一氧化氮合酶、p38MAPK、Caspase-3介导缺氧神经细胞凋亡机制的研究[J].中华实验外科杂志,2007,24(2):213-215. 被引量:21
  • 3杨卫忠,陈春美,王春华,石松生,雷军荣,张永亮.一氧化氮和一氧化氮合酶在大鼠局灶性脑缺血中的表达特点[J].中国神经精神疾病杂志,2007,33(6):335-339. 被引量:38
  • 4Dudek H, Datta S R, Franke T F, et al. Regulation of neuronal survival by the serine-threonine protein kinase Akt [ J ]. Science, 1997, 275(5300) :661 -5.
  • 5Takuwa Y. Rho-Rho kinase pathway [ J ]. Nippon Rinsho, 2004,62 (1) :43 -8.
  • 6Shi J, Wei L. Rho kinase in the regulation of cell death and survival [ J]. Arch Immunol Ther Exp(Warsz) ,2007,55(2 ) :61 - 75.
  • 7Rikitake Y, Kim H H, Huang Z, et al. Inhibition of Rho kinase (ROCK) leads to increased cerebral blood flow and stroke protection[ J]. Stroke,2005,36(10) :2251 -7.
  • 8Satoh S, Utsunomiya T, Tsurui K, et al. Pharmacological profile of hydroxy fasudil as a selective rho kinase inhibitor on ischemic brain damage [ J ]. Life Sci ,2001,69 (12) : 1441 - 53.
  • 9Longa E Z, Weinstein P R, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats[ J]. Stroke, 1989, 20(1) :84 -91.
  • 10Ouyang Y B, Tan Y, Comb M, et al. Survival-and death-promoting events after transient cerebral ischemia:phosphorylation of Akt, release of cytochrome C and Activation of caspase-like proteases[ J]. J Cereb Blood Flow Metab,1999,19(10) :1126-35.

共引文献22

同被引文献54

  • 1吴晓燕.人参总皂甙对大鼠缺血再灌注后神经元凋亡的保护及作用机制的研究[J].神经疾病与精神卫生,2005,5(5):347-350. 被引量:15
  • 2赵燕玲,曲友直,王宗仁.芪丹通脉片及拆方对脑缺血再灌注后神经细胞凋亡及Bcl-2蛋白表达的影响[J].中华老年心脑血管病杂志,2006,8(2):133-135. 被引量:9
  • 3Fu H Li W Lao Y Luo J Lee NT Kan KK Tsang HW Tsim KW Pang Y Li Z Chang DC Li M Han Y.Bis(7)-tacrine attenuates beta amyloid-induced neuronal apoptosis by regulating L-type calcium channels[J].中国生物学文摘,2006,20(10):7-8. 被引量:10
  • 4Yamashima T, Zhao L, Wang XD, et al. Neuroprotective effects of pyridoxal phosphate and pyridoxal against ischemia in monkeys. Nutr Neurosci, 2001, 4(5): 389-397.
  • 5Chaitanya GV, Babu PP. Multiple apoptogenic proteins are involved in the nuclear translocation of Apoptosis Inducing Factor during transient focal cerebral ischemia in rat. Brain Res, 2008, 1246: 178-190.
  • 6Benchoua A, Braudeau J, Reis A, et al. Activation of proinflammatory caspases by cathepsin B in focal cerebral is- chemia. J Cereb Blood Flow Metab, 2004, 24 (11 ) : 1272-1279.
  • 7Tsubokawa T, Solaroglu I, Yatsushige H, et al. Cathepsin and calpain inhibitor E64d attenuates matrix metalloprotein- ase-9 activity after focal cerebral ischemia in rats. Stroke, 2006, 37(7): 1888-1894.
  • 8Windelborn JA, Lipton P. Lysosomal release of cathepsins causes isehemic damage in the rat hippocampal sliee and de- pends on NMDA-mediated caleium influx, araehidonic aeid metabolism, and free radical production. J Neuroehem, 2008, 106(1) : 56-69.
  • 9Yamashima T. Ca^2 + -dependent proteases in ischemic neuro- nal death: a conserved ' calpain-cathepsin cascade' from nematodes to primates. Cell Calcium, 2004, 36 ( 3-4 ) : 285 -293.
  • 10Taha TA, Kitatani K, Bielawski J, et al. Tumor necrosis factor induces the loss of sphingosine kinase-1 by a cathepsin B-dependent mechanism. J Biol Chem, 2005, 280 (17) : 17196-17202.

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