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目的探讨microRNA-211-5p(miR-211-5p)在阿尔茨海默病(Alzheimers disease,AD)模型小鼠脑组织中及体外细胞模型中的表达情况。方法 APPswe/PS1ΔE9双转基因小鼠21只为观察组,野生型C57BL/6J小鼠21只为正常对照组,2组2、4、6、9、12、15、18个月龄小鼠均各有3只,分别提取2组各个月龄小鼠脑皮层及海马组织总RNA,采用TaqMan探针荧光定量PCR技术检测脑组织中miR-211-5p表达水平。美国癌症研究所小鼠胚胎E18.5d脑皮层神经元体外原代培养7d后分为溶剂对照组和β-淀粉样肽(β-amyloid peptide,Aβ)处理组,Aβ处理组采用Aβ1-42处理,溶剂对照组采用DMSO处理,处理0、12、24h后采用SYBR Green相对荧光定量PCR方法检测2组miR-211-5p表达水平。结果观察组9、12、15、18个月龄小鼠脑皮层组织中miR-211-5p表达水平(2 003.62±385.36、399.67±112.79、4 310.67±900.12、7 994.76±2 061.93)均明显高于对照组(1 305.53±203.72、184.77±71.50、1 077.95±81.13、3 176.20±1 629.84)(P<0.05),海马组织miR-211-5p表达水平与对照组比较差异无统计学意义(P>0.05);处理12、24h后,Aβ处理组miR-211-5p表达水平(ct值:12.35±1.52、13.08±1.84)明显高于溶剂对照组(ct值:13.15±1.55、13.48±1.73)(P<0.05)。结论 AD模型小鼠脑皮层组织miR-211-5p表达水平升高,miR-211-5p可能参与AD认知障碍的发生。
Objective To investigate the expression of microRNA-211-5p (miR-211-5p) in the brain of Alzheimer’s disease (AD) model mice and in vitro cell models. METHODS: Twenty-one APPswe / PS1ΔE9 double transgenic mice were selected as observation group, 21 wild-type C57BL / 6J mice as normal control group, 2, 4, 6, 9, 12, The total RNA was extracted from the cerebral cortex and hippocampus of two groups of mice at each month. The expression of miR-211-5p in brain tissue was detected by TaqMan probe real-time PCR. The primary culture of cerebral cortical neurons of mouse embryos E18.5d of the American Cancer Institute was divided into solvent control group and β-amyloid peptide (Aβ) treatment group, and Aβ1-42 treatment group The solvent control group was treated with DMSO, and the expression of miR-211-5p in the two groups was detected by SYBR Green relative fluorescence quantitative PCR after treatment for 0, 12 and 24 hours. Results The expression of miR-211-5p in the cortex of 9, 12, 15 and 18 months old mice in the observation group was significantly higher than that in the control group (2 003.62 ± 385.36, 399.67 ± 112.79, 4 310.67 ± 900.12 and 7 994.76 ± 2 061.93) There was no significant difference in the expression of miR-211-5p in the hippocampus between the control group and the control group (P <0.05), P <0.05 (P <0.05) > 0.05). The expression of miR-211-5p (ct: 12.35 ± 1.52, 13.08 ± 1.84) in Aβ group was significantly higher than that in solvent group after 12 and 24 hours treatment (ct values: 13.15 ± 1.55 and 13.48 ± 1.73) (P <0.05). Conclusion The expression of miR-211-5p in cortex of AD model mice is increased, and miR-211-5p may be involved in the development of AD cognition.