双酚A通过长非编码RNA X非活性特异性转录物和MicroRNA-34a-5p途径调节年龄相关性听力损失

Shifei Wang, C. Rao, Xin-Qiong Huang, Tianhong Xie, Linling Su, Huan Li
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引用次数: 0

摘要

年龄相关性听力损失(AHL)是世界范围内老年人常见的、高发的感知疾病。由于双酚A(BPA)已被报道与细胞凋亡有关,我们假设BPA可以抑制AHL中的神经元凋亡。招募40只Wistar大鼠建立AHL模型;然后用不同剂量的BPA对它们进行处理。我们使用听觉脑干反应测试来测量BPA诱导的大鼠听力改善。我们用MTT法和流式细胞术检测了大鼠听皮层神经元的增殖和凋亡。此外,为了阐明BPA对AHL影响的潜在机制,我们用一种名为纳米颗粒PCR的新方法定量了大鼠听觉皮层中长非编码RNA X无活性特异性转录物(lncRNA XIST)和miR-34a-5p的表达水平。我们发现BPA干预改善了AHL模型大鼠的听力,增强了神经元细胞增殖,限制了神经元细胞凋亡,上调了miR-34a-5p水平,下调了lncRNA XIST水平。双荧光素酶报告子(DLR)测定显示,BPA通过用lncRNA XIST靶向miR-34a-5p来抑制听觉皮层神经元的凋亡,并调节AHL的过程。因此,我们得出结论,BPA有助于AHL的改善,这可能是通过上调miR-34a-5p和通过lncRNA XIST抑制听觉皮层神经元的凋亡来实现的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Regulating Age-Related Hearing Loss with Bisphenol A via the Long Non-Coding RNA X Inactive Specific Transcript and MicroRNA-34a-5p Pathways
Age-related hearing loss (AHL) is a common, high-incidence, perceptual disease in the elderly population worldwide. Since bisphenol A (BPA) has been reported to associate with cell apoptosis, we hypothesize that BPA can inhibit the neuronal apoptosis in AHL. Forty Wistar rats were recruited to model AHL; they were then treated with different doses of BPA. We used auditory brainstem response testing to measure the BPA-induced improvement in the rats’ hearing. We examined the proliferation and apoptosis of the auditory cortical neurons in the rats with MTT assay and flow cytometry. Also, to delineate the underlying mechanism of BPA’s effect on AHL, we quantitated the expression level of long non-coding RNA X inactive specific transcript (lncRNA XIST) and miR-34a-5p in the rats’ auditory cortex with a novel method called nanoparticle PCR. We found that BPA intervention improved the hearing of AHL model rats, enhanced neuronal cell proliferation, restricted neuronal cell apoptosis, upregulated miR-34a-5p levels, and downregulated lncRNA XIST levels. The dual-luciferase reporter (DLR) assay revealed that BPA inhibited the apoptosis of auditory cortex neurons by targeting miR-34a-5p with lncRNA XIST and regulated the process of AHL. Therefore, we come to a conclusion that BPA contributes to the improvement of AHL, which may be achieved by upregulating miR-34a-5p and inhibiting the apoptosis of auditory cortex neurons via lncRNA XIST.
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来源期刊
Nanoscience and Nanotechnology Letters
Nanoscience and Nanotechnology Letters Physical, Chemical & Earth Sciences-MATERIALS SCIENCE, MULTIDISCIPLINARY
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