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大脑中动脉闭塞大鼠继发丘脑损害与NAD含量关系探讨
The relationship of NAD to secondary thalamus damage of the MCAO rats
【摘要】 目的观察大脑中动脉闭塞(MCAO)大鼠继发性丘脑病变,探讨其与NAD含量改变的关系,并考察缺血48 h后补充外源性NAD+能否减轻损害程度。方法建立5组动物分组,分别为MCAO模型组、建模48 h后补充NAD+组(NAD组)、建模48 h后补充溶剂组(溶剂组)、假手术组和空白对照组。采用线栓法制作大鼠大脑中动脉闭塞模型,并于建模48 h后向NAD组腹腔注射NAD+50 mg/kg,同时向溶剂组腹腔注射等量0.9%Na Cl溶液。于建模4周后处死大鼠,取丘脑行免疫组化,测定β淀粉样蛋白前体(APP)表达情况,尼氏染色计数形态完整细胞数,并使用酶循环法测定丘脑NAD含量。结果与假手术组、空白对照组比较,模型组APP表达较高,NAD含量及完整神经元个数减少(P<0.05)。与模型组比较,NAD组APP表达较低,NAD含量及完整神经元个数较高(P<0.05)。结论大脑中动脉供血区发生局部脑缺血后,丘脑处存在继发性病变。NAD含量变化与继发性丘脑损害相关。脑梗死48 h后补充外源性NAD+能够减轻丘脑损害。
【Abstract】 Objective To explore relationship between the decrease of NAD and the remote damage after cerebral ischemia,and the effect of administration with NAD+on the damage. Methods Experimental animals were divided into middle cerebral artery occlusion( MCAO) group,NAD group,solvent group,sham-operated group and normal control group. Making the MCAO model by using the inserting thread method,and NAD+( 50 mg/kg) or 0. 9% Na Cl was administered intraperitoneally to the rats 48 hours after ischemia.The rats were put to death after 4 weeks of MCAO to obtain the thamalus which were analyzed by nissle staining,immunohistochemistry analysis of the expression of β-amyloid precursor protein( APP) and the NAD level detection. Results Compared with the other groups,the expression of APP in the MCAO group was higher,and the NAD level and the number of intact neurons was lower( P <0. 05). Compared with the MCAO group,the expression of APP in NAD group was lower,and the NAD level and the number of intact neurons was higher( P < 0. 05). Conclusion There is secondary damage at thalamus after the local ischemia within the middle cerebral artery blood supplied zone. The NAD level is correlated with the thamalus damage of MCAO rats. Administration with the NAD+after brain ischemia may reduce the damage.
【Key words】 Middle cerebral artery occlusion; Secondary remote damage; NAD; Cerebral infarction; APP;
- 【文献出处】 临床军医杂志 ,Clinical Journal of Medical Officers , 编辑部邮箱 ,2016年04期
- 【分类号】R743.3
- 【被引频次】2
- 【下载频次】105