Alzheimer's disease (AD) is a neurodegenerative disease. Thioredoxin and thioredoxin-interacting protein (TXNIP) complexes help sustain cell oxidation/reduction balance. In the present study, we verified the neuroprotective role of estradiol against amyloid-beta 42 in SH-SY5Y cells through inhibiting TXNIP expression, promoting cell viability and DNA synthesis ability, inhibiting cell apoptosis, and affecting caspase and Bax/Bcl-2 apoptotic signaling. miR-106b-5p could bind to TXNIP 3′-untranslated region to inhibit the expression level of TXNIP. Within SH-SY5Y cells, miR-106b-5p inhibition repressed cell viability and DNA synthesis ability and promoted cell apoptosis through caspase and Bax/Bcl-2 apoptotic signaling, while miR-106b-5p overexpression or TXNIP knockdown exerted the opposite effects on SH-SY5Y cells; TXNIP knockdown remarkably attenuated the roles of miR-106b-5p inhibition. In conclusion, estradiol treatment on SH-SY5Y cells downregulates TXNIP expression and upregulates miR-106b-5p expression. miR-106b-5p exerts a neuroprotective effect on SH-SY5Y cells by promoting cell proliferation and inhibiting cell apoptosis through targeting TXNIP.

中文翻译：

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雌二醇通过 miR-106b-5p/TXNIP 轴对 SH-SY5Y 细胞产生神经保护作用

阿尔茨海默病 (AD) 是一种神经退行性疾病。硫氧还蛋白和硫氧还蛋白相互作用蛋白 (TXNIP) 复合物有助于维持细胞氧化/还原平衡。在本研究中，我们通过抑制 TXNIP 表达、促进细胞活力和 DNA 合成能力、抑制细胞凋亡以及影响 caspase 和 Bax/Bcl-2 凋亡信号传导，验证了雌二醇对 SH-SY5Y 细胞中淀粉样蛋白 42 的神经保护作用. miR-106b-5p 可以结合 TXNIP 3'-非翻译区以抑制 TXNIP 的表达水平。在 SH-SY5Y 细胞内，miR-106b-5p 抑制通过 caspase 和 Bax/Bcl-2 凋亡信号抑制细胞活力和 DNA 合成能力并促进细胞凋亡，而 miR-106b-5p 过表达或 TXNIP 敲低对 SH 产生相反的影响-SY5Y 细胞；TXNIP 敲低显着减弱了 miR-106b-5p 抑制的作用。总之，雌二醇处理 SH-SY5Y 细胞会下调 TXNIP 表达并上调 miR-106b-5p 表达。miR-106b-5p通过靶向TXNIP促进细胞增殖和抑制细胞凋亡，从而对SH-SY5Y细胞发挥神经保护作用。