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首页> 外文期刊>Journal of applied toxicology >Microarray profile analysis of toxic cocaine-induced alterations in the expression of mouse brain gene sequences: a possible 'protective' effect of buprenorphine.
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Microarray profile analysis of toxic cocaine-induced alterations in the expression of mouse brain gene sequences: a possible 'protective' effect of buprenorphine.

机译:毒性可卡因诱导的小鼠脑基因序列表达变化的微阵列谱分析:丁丙诺啡可能的“保护”作用。

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摘要

Using a mouse brain cDNA microarray consisting of 2688 gene sequences, which include unknown sequences with the empirical possibility of expression in the brain, the effects of repeated toxic doses of intraperitoneal (i.p.) cocaine (40 mg x kg(-1), 4 days) on the expression pro fi le of the cerebral genes were investigated. The modifications in this pro file caused by buprenorphine (BUP) (0.25 mg x kg(-1) i.p., 4 days), a protective drug against cocaine, were also examined. In the cocaine group, the expression levels reached the recommended increased levels (>or=2 times the control value in the saline-treated control group) in 24.0% of the genes but were equal to or less than the recommended attenuation levels (0.5 and <2 times the control value). Although statistically significant modifications in the expression of cocaine- or BUP-related brain-region-specific genes were not proved using whole cerebrums, including many unknown genes, our results suggest that the expression of genes related to neuronal cell damage, including non-peculiar genes related to the damage accompanying convulsive seizures and malignant tumors, were normalized and the genes related to the protection of neural cells were induced by BUP.
机译:使用由2688个基因序列组成的小鼠大脑cDNA微阵列,其中包括具有在大脑中表达的经验可能性的未知序列,反复毒性剂量的腹膜内(ip)可卡因(40 mg x kg(-1),4天)的影响)对大脑基因的表达谱进行了研究。还检查了由丁丙诺啡(BUP)(0.25 mg x kg(-1)i.p.,4天)(一种可卡因的保护性药物)引起的对该文件的修改。在可卡因组中,表达水平在24.0%的基因中达到了建议的增加水平(>或=生理盐水处理对照组的对照值的2倍),但等于或小于建议的衰减水平(<或在14.0%的基因中是对照值的0.5倍)。在可卡因-BUP组中,总基因的其他15.4%的表达水平升高,而总基因的其他18.2%的表达水平降低。但是,与BUP降低的死亡率和癫痫发作的严重程度相对应,具有高于背景水平的可卡因修饰基因的80.1%的表达水平恢复到推荐的正常水平(> 0.5且<2倍于对照值)。尽管使用整个大脑,包括许多未知基因,未证明可卡因或BUP相关脑区域特异性基因表达的统计学上显着改变,但我们的结果表明与神经元细胞损伤有关的基因(包括非特有的)的表达将与惊厥性癫痫发作和恶性肿瘤相关的损伤相关基因进行标准化,并通过BUP诱导与保护神经细胞相关的基因。

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