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AIM and METHODS: The ratio of mitochondrial DNA (mtDNA) deletion was measured to find the relationship between mtDNA deletion and aged learning and memory deficit. The aged rats were divided into two groups, aged learning and memory deficit group and aged learning and memory normal group. The ratio of mtDNA deletion was measured by dilution polymerase chain reaction. RESULTS: There are deleted mtDNA (about 4834 bp) in the cerebral cortex, hippocampus and cerebellum of both young and aged rats. The ratios of deleted mtDNA were similar in the cerebral cortex,hippocampus and cerebellum of young rats (about 0.00018%). The ratio mtDNA of aged learning and memory normal rats had increased by five-fold in the cerebral cortex and hippocampus, or one-fold in the cerebellum over young rats. The ratio of aged learning and memory dificit rats had increased by one-fold in the cerebral cortex or 0.8-fold in the hippocampus or two-fold in the cerebellum over aged learning and memory normal rats.CONCLUSIONS: There was really the increase of mtDNA in aging rat brain. And this increase was double in amount in aged learning and memory deficit rats compared to the normal learning and memory aged rats. It is suggested that the mtDNA deletions in the brain regions associated with learning and memory may be contributed to the cellular and molecular mechanism of learning and memory deicit with aged rats. 相似文献
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AIM To investigate the activation of related repair pathways after bupivacaine-induced neuronal DNA damage by cDNA gene screening. METHODS The bupivacaine-induced SH-SY5Y neuronal damage and DNA damage model was established. The technique of cDNA microplate array was used to screen the 21 important regulatory factors in the DNA damage repair pathway. Post-analysis of these differentially expressed repair genes for the repair pathway enrichment and distribution was performed. The data were analyzed by GraphPad Prism 6 statistical software to compare differences between groups. RESULTS The viability of SH-SY5Y cells treated with bupivacaine at different concentrations (detected by CCK-8 assay) showed that the IC50 value of bupivacaine was 1.5 mmol/L. The comet assay related index (the comet tail) was increased (P <0.05), the phosphorylation level of γH2AX protein was increased (P <0.05), indicating that DNA damage in the SH-SY5Y cells was significantly aggravated after bupivacaine treatment. The results of cDNA microplate assay showed that compared withcontrol group, the differentially expressed genes after bupivacaine treatment were DNA-PKcs , PTEN , NTH1 , RAD9 , CSB , GADD45 , XPD, XPC-HR23B and P53 . The analysis showed that these repair genes were mainly concentrated in the following 3 repair mechanisms: base excision repair, nucleotide excision repair, and non-homologous reconstitution. CONCLUSION The repair genes differentially expressed after neuronal DNA damage caused by local anesthetics are mainly concentrated in the pathways of non-homologous end-joining, base excision repair and nucleotide excision repair. 相似文献
75.
苹果RAPD分析体系的建立 总被引:3,自引:0,他引:3
对富士苹果(Malus pumila Mill.cv.Fuji)RAPD(Random Amplified Polymorphic DNA)分析体系的优化研究表明,RAPD反应体系中,DNA、Taq酶、引物和Mg2+4种主要成分的最适用量分别为:20ng、1.0 U、0.2umol·L-1和3.0umol·L-1。采用该优化体系,以 OPJ03为引物,构建了我国及世界范围内苹果生产中重要的28个品种的RAPD指纹图谱,分析了其遗传多样性,区分了供试的28个苹果品种中的15个,区分率达53.6%。讨论了RAPD鉴定苹果品种的应用及其主要影响因素。 相似文献
76.
大豆胞囊线虫病(Heterodera glycines,soybean cyst nematode,SCN)是大豆生产上的重要病害,其特点为危害重、分布广、难防治,每年对大豆生产造成极大的损失。种植大豆抗性新品种是防治SCN目前最为有效的措施,研究大豆对SCN侵染的应答机制,是培育大豆持久抗病品种的前提,对加快抗线虫品种选育及SCN的防控具有重要的意义。本文综述了大豆对SCN侵染的组织细胞学应答机制;介绍了大豆在SCN侵染后酶系变化及酚类代谢的生理生化应答机制;从分子水平阐明了SCN侵染后大豆的基因转录变化,差异蛋白及DNA甲基化的应答机制,以期为大豆胞囊线虫病害的进一步研究与防治提供参考。 相似文献
77.
甜菜DAMD-PCR体系的建立及优化 总被引:2,自引:2,他引:0
为了建立甜菜DAMD扩增体系,以期利用DAMD引物应用于甜菜品种指纹图谱的构建及分子标记辅助育种。本实验利用单因素变量的方法对甜菜DAMD体系进行优化。同时选用12个甜菜品种,利用优化的体系对25条DAMD引物进行扩增。获得甜菜的最适DAMD体系:总体积为20μL,包含模板DNA 10~80 ng、0.75 U的DNA聚合酶、0.2μL的d NTPs(2.5 mmol/L each)以及2.0μL的引物(10μmol/L)。同时25条引物均扩增出了清晰条带,除了个别引物多态性较差外,其余引物多态性都非常的丰富,其中引物62H(-)就可以把实验中用到的12个甜菜品种全部区分开。由此可见,DAMD引物的扩增效率很高,并且扩增结果稳定,条带清晰,非常适合甜菜品种指纹图谱的构建及遗传多样性分析。 相似文献
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79.
以35份富士苹果(Malus×domestica Borkh.‘Fuji’)芽变材料为试材,利用甲基化敏感扩增多态性(Methylation Sensitive Amplified Polymorphism,MSAP)分析和UPGMA聚类方法,对其基因组甲基化修饰水平、变异模式以及表观遗传变异关系进行研究。结果表明:(1)不同富士系得到不同的MSAP扩增,总DNA甲基化水平27.90%~36.16%,平均32.87%,双链全甲基化为主要甲基化方式;(2)富士芽变材料绝大多数位点保持了原有甲基化模式;(3)绝大多数芽变(68.57%)检测到全部的甲基化变异模式(12种),去甲基化频率极显著高于甲基化频率(P <0.01),且CG去甲基化极显著高于CHG;(4)36份种质遗传相似系数平均值0.89(0.79~0.92),在聚类图上,富士原种分布在芽变系集中区外,新近发生的芽变系更倾向于聚在一起,着色系片红型和条红型芽变呈分散排布状态。总的来看,富士芽变的甲基化变异模式丰富,超甲基化和去甲基化相伴发生,但以去甲基化为主;‘富士’着色芽变与其最原始品种富士,以及芽变之间发生了较大表观遗传变异;片红和条红型芽变聚类未表现明显偏好性。本研究将为进一步开展富士着色系芽变机理研究提供指导,可以CG去甲基化为切入点展开深入研究。 相似文献
80.
JIAO Peng HUANG Zhen-zhou ZHANG Xiao-jing LONG Yan-jun LI Zhao-jun WANG Feng-ze 《园艺学报》2019,35(2):260-266
AIM:To investigate the effect of CUDC-907, a dual histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K) inhibitor, on the DNA damage, cell cycle distribution and autophagy in human glioma U251 cells. METHODS:U251 cells were treated with CUDC-907 of different concentrations, and the cell viability was detected by MTT assay. The quantitative γ-H2AX foci were determined by laser scanning confocal microscopy. The cell cycle distribution of U251 cells was examined by flow cytometry. The protein expression was determined by Western blot analysis. RESULTS:CUDC-907 inhibited the cell viability and the phosphorylation of Akt and p70 ribosomal protein S6 kinase (p70s6K) in the U251 cells (P<0.05). In CUDC-907-treated cells, the number of γ-H2AX foci and protein expression of γ-H2AX were increased significantly (P<0.05). CUDC-907 also induced cell arrest in the G2/M phase by up-regulating the expression of p21, and inhibiting the protein level of cyclin B1 and the phosphorylation of cell division cycle protein 2 (Cdc2). In addition, CUDC-907 triggered cell autophagy, and inhibition of autophagy increased CUDC-907-induced DNA damage of U251 cells. CONCLUSION:CUDC-907 significantly inhibits PI3K/Akt signaling pathway, induces DNA damage and arrests cell cycle in G2/M phase. Blockage of autophagy promotes CUDC-907-induced DNA damage of U251 cells. 相似文献