RETRACTED: microRNA-139-5p alleviates neurological deficit in hypoxic-ischemic brain damage via HDAC4 depletion and BCL-2 activation
| Autor: | Sheng Li, Shinuan Fei, Lichun Cao |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Apoptosis Inflammation Brain damage Oxidative phosphorylation medicine.disease_cause Histone Deacetylases Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Internal medicine microRNA medicine Animals Neurons Gene knockdown business.industry General Neuroscience Brain HDAC4 Rats Up-Regulation Disease Models Animal MicroRNAs Oxidative Stress 030104 developmental biology Endocrinology Proto-Oncogene Proteins c-bcl-2 Hypoxia-Ischemia Brain medicine.symptom business 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Brain Research Bulletin. 169:73-80 |
| ISSN: | 0361-9230 |
| DOI: | 10.1016/j.brainresbull.2020.12.020 |
| Popis: | Aim Studies paid much attention to the role of microRNAs (miRNAs) in hypoxic-ischemic brain damage (HIBD) but not much to miR-139−5p. Thus, this study is to uncover the potential role of miR-139−5p in HIBD and its mechanisms. Methods Rat HIBD models were established by Rice-Vannucci method. Rats were injected with miR-139−5p agomir and si-histone deacetylase 4 (HDAC4) to explore their roles in HIBD. For further verification, growth and development assessments, and neurological behavior test were conducted. Oxidative stress-related factors, miR-139−5p, HDAC4 and B-cell lymphoma 2 (Bcl-2) expression in brain tissues and serum inflammatory response were detected. Results MiR-139−5p and Bcl-2 were decreased while HDAC4 was elevated in brain tissues of rats with HIBD. Growth and neurological behaviors were restrained in rats with HIBD. MiR-139−5p up-regulation or HDAC4 down-regulation alleviated pathological status, impaired oxidative stress, increased NGF and BDNF expression and inhibited neurons apoptosis of brain tissues in rats with HIBD. Increased miR-139−5p or decreased HDAC4 impaired inflammation in serum of rats with HIBD. Conclusion Our study highlights that miR-139−5p elevation or HDAC4 knockdown alleviated neurological deficit and induced neurons growth via Bcl-2 elevation. |
| Databáze: | OpenAIRE |
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