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首页> 外文期刊>Journal of cellular biochemistry. >Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway
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Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

机译：通过MAPK信号通路靶向VAV1，MicroRNA-330对淀粉样蛋白β-蛋白质产生，氧化应激和线粒体功能障碍的保护作用

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Abstract This study aims to explore the effect of miR‐330 targeting VAV1 on amyloid β‐protein (Aβ) production, oxidative stress (OS), and mitochondrial dysfunction in Alzheimer's disease (AD) mice through the MAPK signaling pathway. Putative targeted gene of miR‐330 was performed by a miRNA target prediction website and dual‐luciferase reporter gene assay. AD mouse model was successfully established. Fourteen C57 mice were randomized into AD and control groups. The positive protein expression rate of VAV1 was measured by immunohistochemistry. Neuron cells were assigned into control, blank, negative control (NC), miR‐330 mimics, miR‐330 inhibitors, siRNA‐VAV1, and miR‐330 inhibitors?+?siRNA‐VAV1 groups. Expression of miR‐330, VAV1, ERK1, JNK1, P38MAPK, Aβ, COX, and lipoprotein receptor‐related protein‐1 (LRP‐1) were determined using RT‐qPCR and Western blotting. Colorimetry was applied to measure the levels of OS parameters of superoxide dismutase (SOD) and malondialdehyde (MDA). Aβ production in brain tissue was detected using ELISA, while that in neuron cell was measured by radioimmunoassay. MiR‐330 was down‐regulated in neuron cells of AD mice and VAV1 was negatively regulated by miR‐330. Compared with the control group, the positive protein expression rate of VAV1 was significantly elevated in the AD group. Overexpression of miR‐330 decreased the expression of VAV1, ERK1, JNK1, P38MAPK, and Aβ, but increased the expression of COX and LRP‐1. AD mice revealed elevated Aβ production and MDA with decreased SOD level. The result indicates that overexpressed miR‐330 targeting VAV1 through the MAPK signaling pathway reduces Aβ production and alleviates OS and mitochondrial dysfunction in AD.
机译：摘要本研究旨在通过MAPK信号通路探讨靶向VAV1的miR-330对阿尔茨海默病（AD）小鼠淀粉样β蛋白（Aβ）产生、氧化应激（OS）和线粒体功能障碍的影响。通过miRNA靶点预测网站和双荧光素酶报告基因分析来检测miR-330的假定靶基因。成功建立AD小鼠模型。将14只C57小鼠随机分为AD组和对照组。免疫组化检测VAV1阳性蛋白表达率。将神经元细胞分为对照组、空白组、阴性对照组（NC）、miR-330模拟物、miR-330抑制剂、siRNA-VAV1和miR-330抑制剂？+？siRNA-VAV1组。miR-330、VAV1、ERK1、JNK1、P38MAPK、Aβ、COX和脂蛋白受体相关蛋白-1（LRP-1）的表达通过RT-qPCR和Western blotting测定。采用比色法测定超氧化物歧化酶（SOD）和丙二醛（MDA）的OS参数水平。用ELISA法检测脑组织中Aβ的产生，用放射免疫法检测神经元中Aβ的产生。MiR-330在AD小鼠的神经元细胞中下调，VAV1受MiR-330负调控。与对照组相比，AD组VAV1的阳性蛋白表达率显著升高。miR-330的过度表达降低了VAV1、ERK1、JNK1、P38MAPK和Aβ的表达，但增加了COX和LRP-1的表达。AD小鼠的Aβ生成和MDA水平升高，SOD水平降低。结果表明，通过MAPK信号通路靶向VAV1的过表达miR-330可减少Aβ的产生，减轻AD患者的OS和线粒体功能障碍。

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