国际精神病学杂志--大牛智慧平台

您当前位置：首页 > 刊期目次

刊期目次

X-42在Wistar大鼠血管性痴呆模型中海马区的表达及丁苯酞干预的研究

姚娟,高小平

通讯作者: 高小平，

单位：湖南省人民医院 410002

PDF

403

下载量

902

浏览量

引用本文: 姚娟,高小平.X-42在Wistar大鼠血管性痴呆模型中海马区的表达及丁苯酞干预的研究[J]. 国际精神病学杂志, , (): -

【摘要】

目的：检测Wistar大鼠血管性痴呆模型中小胶质细胞表面补体III型受体OX-42在脑海马组织中的动态变化，探讨其在血管性痴呆中的作用。研究丁苯酞对Wistar大鼠血管性痴呆模型中OX-42的影响，阐明丁苯酞可能的机制。
方法：双侧颈总动脉永久结扎术（2-VO）建立Wistar大鼠血管性痴呆模型。设立正常对照组、假手术组、VD模型组、药物干预组。水迷宫试验对大鼠进行学习和记忆成绩测试。应用免疫组织化学法
方法检测OX-42的表达。
结果：模型组大鼠学习和记忆成绩下降，海马区OX-42的表达较正常对照组、假手术组均明显增加（P<0.05）；药物干预组大鼠学习记忆能力明显改善，海马区OX-42的表达下降，与模型组比较差异有统计学意义（P<0.05）。
结论：慢性脑缺血血管性痴呆大鼠海马区OX-42表达升高；丁苯酞可能通过抑制了血管性痴呆大鼠海马区OX-42的表达，从而改善大鼠的学习记忆能力。

【关键词】

血管性痴呆；OX-42；丁苯酞；Wistar大鼠

【Abstract】

Objective: To investigate the dynamic variation of OX-42 in hippocampus tissue after vascular dementia(VD) model in Wistat rats, to explore their effects in vascular dementia. To investigate the effects of Butylphthalide(NBP) on OX-42 after VD model in rats, and clarify the possible mechanism of NBP. Method: The vascular dementia model in Wistar rats were established by permanent bilateral common carotid artery occlusion method. Wistar rats were divided into 4 groups: normal group, sham-operated group, VD model group and NBP treatment group. Then the learning and memory capabilities of rats were tested by Morris water maze. Meanwhile, the expression of OX-42 were measured with methods of immunohistochemistry.
Results: Compared with the normal group and sham-operated group, the abilities of learning and memory apparently decresed in VD model group, and the expression of OX-42 significantly increased in VD model group（P<0.05）. Besides, NBP treatment group significantly improved learning and memory abilities, and compared with the VD model group, the expression of OX-42 significantly reduced in NBP treatment group (P <0.05).
Conclusion : OX-42 expression were significantly increased in hippocampus of chronic cerebral ischemia rats．Butylphthalide might reduced expression of OX-42, and could improve learning and memory abilities of VD rats.

【Key words】

vascular dementia; OX-42; Butylphthalide; Wistar rat

[1] [1]Kettenmann H, Hanisch UK, Noda M, Verkhratsky A. Physiology of microglia[J][J]. Physiol Rev, 2011, 91(): 461–553-.

[2] [2]Dheen ST, Kaur C, Ling EA. Microglial activation and its implications in the brain diseases[J][J]. Curr Med Chem, 2007, 14(): 1189-1197.

[3] [4]Liu B, Gao HM, Hong JS. Parkinson's disease and exposure to infectious agents and pesticides and the occurrence of brain injuries: role of neuroinflammation[J][J]. Environ Health Perspect, 2003, 111(): 1065-1073.

[4] [5]王松柏, 姚咏明, 董宁, 等. JAK/STAT通路介导脓毒症大鼠肝组织高迁移率族蛋白B1mRNA表达的研究[J][J]. 中国危重病急救医学, 2003, 15(): 147-149.

[5] [6]Scaffidi P, Misteli T, Bianchi ME. Release of chromatin protein HMGB1 by necroticcells triggers inflammation[J][J]. Nature, 2002, 418(): 191-195.

[6] [7]Yang H, Wang H, Czura C, et al. The cytokine activity of HMGB1[J][J]. J Leukoc Biol, 2005, 78(): 1-8.

[7] [8]Yang QW, Wang JZ, Li JC, et al. High-mobility group protein box-1 and its relevance to cerebral ischemia[J][J]. J Cereb Blood Flow Metab, 2010, 30(): 243-254.

[8] [9]Walter L, Neumann H. Role of microglia in neuronal degeneration and regeneration[J][J]. Semin Immunopathol, 2009, 31(): 513-525.

[9] [10]Nakajima K, Kohsaka S. Microglia:activation and their significance in the central nervous system[J][J]. Biochem, 2001, 130(): 169-175.

[10] [11]Lotze MT,Tracey KJ. High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal[J][J]. Nat Rev Immunol, 2005, 5(): 331-342.

[11] [12]Dumitriu IE, Baruah P, Manfredi AA,et al. HMGB1: guiding immunity from within[J][J]. Trends Immunol, 2005, 26(): 381-387.

[12] [13]Ulloa L,Messmer D. High-mobility group box 1 (HMGB1) protein: friend and foe[J][J]. Cytokine Growth Factor Rev, 2006, 17(): 189-201.

[13] [14]Oppenheim JJ, Yang D. Alarmins: chemotactic activators of immune responses[J][J]. Curr Opin Immunol, 2005, 17(): 359-365.

[14] [15]Bianchi ME. DAMPs, PAMPs and alarmins: all we need to know about danger[J][J]. J Leukoc Biol, 2007, 81(): 1-5.

[15] [16]Wang H, Vishnubhakat JM, Bloom O, et al. Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein-1 by pituicytes[J][J]. Surgery, 1999, 126(): 389-392.

[16] [17]Agnello D, Wang H, Yang H, et al. HMGB-1, a DNA-binding protein with cytokine activity, induces brain TNF and IL-6 production, and mediates anorexia and taste aversion[J][J]. Cytokine, 2002, 18(): 231-236.

[17] [18]O'Connor KA, Hansen MK, Rachal Pugh C, et al. Further characterization of high mobility group box 1 (HMGB1) as a proinflammatory cytokine: central nervous system effects[J][J]. Cytokine, 2003, 24(): 254-265.

[18] [19]Passalacqua M, Patrone M, Picotti GB, et al. Stimulated astrocytes release high-mobility group 1 protein, an inducer of LAN-5 neuroblastoma cell differentiation[J][J]. Neuroscience, 1998, 82(): 1021-1028.

[19] [20]Takata K, Kitamura Y, Tsuchiya D, et al. High mobility group box protein-1 inhibits microglial Abeta clearance and enhances Abeta neurotoxicity[J][J]. J Neurosci Res, 2004, 78(): 880-891.

[20] [21]Goldstein RS, Gallowitsch-Puerta M, Yang L, et al. Elevated high-mobility group box 1 levels in patients with cerebral and myocardial ischemia[J][J]. Shock, 2006, 25(): 571-574.