4.3 Article

A study on the neuroprotective effect of miR-206-3p on Alzheimer's disease mice by regulating brain-derived neurotrophic factor

Journal

ANNALS OF TRANSLATIONAL MEDICINE
Volume 10, Issue 2, Pages -

Publisher

AME PUBL CO
DOI: 10.21037/atm-21-6601

Keywords

MicroRNA-206-3p (miR-206-3p); Alzheimer's disease (AD); brain-derived neurotrophic factor (BDNF); neurons

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This study found that miR-206-3p is involved in the neuroprotective effect of AD mice by regulating BDNF. Intervening with miR-206-3p mimics led to increased expression of miR-206-3p, improving cognitive and motor function in AD mice, promoting the recovery of neuron morphology, and increasing the expression of BDNF protein.
Background: Brain-derived neurotrophic factor (BDNF) is involved in the regulation of Alzheimer's disease (AD), but the mechanism is not clear. This study explores the possible mechanism of microRNA-206-3p (miR-206-3p) participating in the neuroprotective effect of AD mice by regulating BDNF. Methods: 36 SPF grade C57 mice were randomly divided into normal group, model group and miR-206-3p mimics group (intraperitoneal injection of 3 mm miR-206-3p mimics) (n=12). miR-206-3p mimics group was intervened by miR-206-3p mimics on the basis of AD model. The expression of miR-206-3p was detected by Real time quantitative polymerase chain reaction (qPCR). Zea-Longa score and water maze were used for behavioral detection, he was used to observe the morphology of neurons, and immunohistochemical Western blot was used to detect the expression of BDNF protein, and the targeting relationship between miR-206-3p and BDNF was analyzed. Results: Compared with the model group, the expression level of miR-206-3p in miR-206-3p mimics group was significantly higher (P<0.05). compared with the model group, the Zea-Longa score in miR206-3p mimics group was significantly lower (P<0.05). The escape latency of miR-206-3p mimics group was significantly shorter than that of model group, and the number of crossing the original platform was significantly more than that of model group (P<0.05). The morphology of neurons in miR-206-3p mimics group was significantly better than that in model group; Immunohistochemistry and Western blot showed that the relative expression of miR-206-3p mimics BDNF protein was significantly increased compared with the model group (P<0.05). Compared with miR-206-3p control group, the luciferase activity at 3' end untranslated area (3' UTR) end of wild-type BDNF in miR-206-3p inhibition group decreased significantly (P<0.01). Conclusions: miR-206-3p exerts neuroprotective effects on AD mouse neurons by up-regulating BDNF.

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