Alzheimer’s disease (AD) is the most common cause of dementia among older people in worldwide. miR-29c-3p was reported to play a role in AD development. However, the detail function of miR-29c-3p in AD remains unclear. The aim of this research is to analyze the functional mechanism of miR-29c-3p in AD. The RNA levels of miR-29c-3p and Tumor necrosis factor-α-inducible protein-1 (TNFAIP1) were detected by Quantitative real time polymerase chain (qRT-PCR) reaction. Western blot assay was carried out to examine the protein levels of TNFAIP1, Bax, B-cell lymphoma-2 (Bcl-2), Cleaved caspase 3, and Nuclear factor-k-gene binding (NF-κB). The interaction between miR-29c-3p and TNFAIP1 was predicted by online tool TargrtScan and verified using the dual luciferase reporter assay and RNA immunoprecipitation RIP (RIP) assay. Besides, cell proliferation and apoptosis rate were determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. Aβ treatment decreased miR-29c-3p expression and increased TNFAIP1 expression. Overexpression of miR-29c-3p mitigated the effects of Aβ on proliferation and apoptosis. Similarly, knockdown of TNFAIP1 also reversed the effects of Aβ on cell progression. Interestingly, miR-29c-3p suppressed the expression of TNFAIP1 via binding to 3′UTR of TNFAIP1 mRNA. As expected, overexpression of TNFAIP1 reversed the effects of miR-29c-3p on Aβ-mediated cell progression. Besides, we also confirmed that miR-29c-3p affected Aβ-mediated cell progression by regulating TNFAIP1/NF-κB signaling pathway. In conclusion, our findings confirmed that miR-29c-3p attenuated Aβ-induced neurotoxicity through regulation of NF-κB signaling pathway by directly targeting TNFAIP1, providing the potential value for the treatment of AD patients.

阿尔茨海默氏病（AD）是全世界老年人中最常见的痴呆病原因。据报道，miR-29c-3p在AD发育中起作用。但是，miR-29c-3p在AD中的详细功能仍不清楚。这项研究的目的是分析miR-29c-3p在AD中的功能机制。通过定量实时聚合酶链反应（qRT-PCR）检测miR-29c-3p和肿瘤坏死因子-α诱导型蛋白1（TNFAIP1）的RNA水平。进行了蛋白质印迹分析，以检查TNFAIP1，Bax，B细胞淋巴瘤2（Bcl-2），Cleaved caspase 3和核因子-k基因结合（NF-κB）的蛋白水平。miR-29c-3p与TNFAIP1之间的相互作用是通过在线工具TargrtScan预测的，并使用双重荧光素酶报告基因检测和RNA免疫沉淀RIP（RIP）检测进行了验证。除了，细胞增殖和凋亡率分别通过3-（4,5-二甲基-2-噻唑基）-2、5-二苯基-2-H-溴化四唑（MTT）测定和流式细胞术分析来确定。Aβ处理降低miR-29c-3p表达并增加TNFAIP1表达。miR-29c-3p的过表达减轻了Aβ对增殖和凋亡的影响。同样，敲低TNFAIP1也可以逆转Aβ对细胞进程的影响。有趣的是，miR-29c-3p通过与TNFAIP1 mRNA的3'UTR结合来抑制TNFAIP1的表达。如预期的，TNFAIP1的过表达逆转了miR-29c-3p对Aβ介导的细胞进程的影响。此外，我们还证实了miR-29c-3p通过调节TNFAIP1 /NF-κB信号通路影响Aβ介导的细胞进程。结论，