Evidence map›Paper›PMID 34013967›Full record

ArticleHistology and histopathology2021

Olig2 knockdown alleviates hypoxic-ischemic brain damage in newborn rats.

L J Yang, H Cui

Abstract read
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In one paragraph

Article in Histology and histopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

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0 citing papers in PubMed, 0 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

L J YangDepartment of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, China. ljy20082008@126.com.
H CuiDepartment of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, China. cuihong2017@126.com.
Beijing Friendship Hospital · CNCapital Medical University · CN

Funding

National Natural Science Foundation of China 81771622Natural Science Foundation of Beijing Municipality 7202035
6 · The paper itself

Abstract

objectivesNeuronal damage is an important pathological mechanism in neonatal hypoxic-ischemic brain damage (HIBD). We found in our previous studies that oligodendrocyte transcription factor 2 (Olig2) downregulation was able to increase cell survival in the brain. However, the specific mechanism has yet to be clarified.

methodsSprague-Dawley rats aged 3 d were randomly divided into three groups: the normal control group, the Olig2-RNAi group, and the RNAi-negative control group. The normal control group received no treatment, the Olig2-RNAi group received the Olig2 RNAi adenovirus, and the RNAi-negative control group was given the control adenovirus after the completion of the HIBD model. Infarct lesions and their volumes were observed by triphenyltetrazolium chloride (TTC) staining 3 d after the completion of the adenovirus local injection. The condition of the tissue was characterized by hematoxylin-eosin staining 7 d after the model was established, and cell viability was determined by azure methylene blue staining. Subcellular damage was analyzed by transmission electron microscopy. Rotarod analysis was performed to detect moving behavior ability and an MWM assay was conducted to evaluate the memory.

resultsTTC staining showed a smaller brain injury area in the Olig2-RNAi group than in the RNAi-negative control group. Hematoxylin-eosin staining indicated the presence of severe cell injury in the hippocampal region after HIBD, which improved after Olig2 knockdown. Azure methylene blue staining and electron microscopy results suggested that the cells improved after Olig2 knockdown. The rats stayed longer on the rotating rod, and their latency in the water maze test was gradually shortened relative to that of the rats in the Olig2-RNAi negative control group.

conclusionOlig2 knockdown can promote the repair of hypoxic-ischemic brain damage in newborn rats.

Indexed as

Hypoxia-Ischemia, BrainNeuronsOligodendrocyte Transcription Factor 2AnimalsAnimals, NewbornBrainCerebral CortexDisease Models, AnimalGene Knockdown TechniquesNeuroprotective AgentsRatsRats, Sprague-DawleyRNA InterferenceNeuroprotective AgentsOligodendrocyte Transcription Factor 2

Identifiers

PMID34013967
OpenAlexW3163098847

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.