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Estradiol exerts a neuroprotective effect on SH‐SY5Y cells through the miR‐106b‐5p/TXNIP axis

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.