Abstract: Objective To explore the effect of microRNA-200 a-3 p ( miR-200a-3p) on hypoxic-ischemic brain damage (HIBD) in neonatal rats. Methods Sixty neonatal SD rats were divided into 4 groups: sham operation group, HIBD group, miR-200a-3p antagomir group, and NCantagomir group, 15 cases in each group. The rat neonatal HIBD model was constructed. The expression level of miR-200a-3p in the hippocampus was detected by quantitative PCR. The nerve functionand brain water content were evaluated. The pathological changes and apoptosis of the hippocampal tissues were observed by HE staining and TUNEL staining. The levels of oxidative stress, inflammatory factors, and the expression levels of apoptosis-related proteins were detected by ELISA andWestern blotting. Results Compared with those in the sham operation group, the expression levelof miR-200a-3p in the hippocampus, the score of nerve function, the brain water content, the apoptosis rate of brain cells, the levels of MDA, IL-6, IL-1β, TNF-α and the expression level ofCleaved-Caspase-3 were increased (P < 0. 05), while the levels of SOD, CAT, Bcl-2 / Bax, BDNF and TrkB were decreased in the HIBD group (P < 0. 05) . Compared with those in the NC-antagomir group, the expression level of miR-200a-3p in the hippocampus, the score of nerve function, the brain water content, the apoptosis rate of brain cells, the levels of MDA, IL-6, IL-1β,TNF-α and the expression level of Cleaved-Caspase-3 were decreased (P < 0. 05), while the levels of SOD, CAT, Bcl-2 / Bax, BDNF and TrkB were increased in the miR-200a-3p antagomir group (P < 0. 05 ) . Conclusion InhibitingmiR-200a-3pcan reduce nerve injury in neonatal rats with HIBD, which may be related to the inhibition of apoptosis and oxidative stress, and the regulation of BDNF / TrkB pathway.

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