ArticleZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics2017
[Role of mitophagy in neonatal rats with hypoxic-ischemic brain damage].
Article in Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Hypoxia Triggers BNIP3/BNIP3L-Associated Mitophagy in HT22 Immortalized Hippocampal Neurons: A Temporal Descriptive Study.Biology · 2026Article
- SIRT1-mediated deacetylation of FOXO3 enhances mitophagy and drives hormone resistance in endometrial cancer.Molecular medicine (Cambridge, Mass.) · 2024Article
- Neuroprotection offered by mesenchymal stem cells in perinatal brain injury: Role of mitochondria, inflammation, and reactive oxygen species.Journal of neurochemistry · 2021Review
- The Role of Mitochondrial and Endoplasmic Reticulum Reactive Oxygen Species Production in Models of Perinatal Brain Injury.Antioxidants & redox signaling · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate mitophagy in an animal model of hypoxic-ischemic brain damage (HIBD) and its role in HIBD.
methodsA total of 120 neonatal Sprague-Dawley rats aged 7 days were divided into three groups: sham-operation, HIBD, and autophagy inhibitor intervention (3MA group). The rats in the HIBD group were treated with right common carotid artery ligation and then put in a hypoxic chamber (8% oxygen and 92% nitrogen) for 2.5 hours. Those in the 3MA group were given ligation and hypoxic treatment at 30 minutes after intraperitoneal injection of 2 μL 3MA. Those in the sham-operation group were not given ligation or hypoxic treatment. Single cell suspension was obtained from all groups after model establishment. Immunofluorescence localization was performed for mitochondria labeled with MitoTracker, autophagosomes labeled with LysoTracker, and autophagy labeled with LC3 to observe mitophagy. After staining with the fluorescent probe JC-1, flow cytometry was used to measure mitochondrial membrane potential. TTC staining was used to measure infarct volume. Cytoplasmic proteins in cortical neurons were extracted, and Western blot was used to measure the expression of mitophagy-related proteins.
resultsCompared with the sham-operation group, the HIBD group had a significant reduction in mitochondrial membrane potential (P<0.05), a significant increase in mitophagy (P<0.05), a significant increase in the expression of the proteins associated with the division of the mitochondrial Drp1 and Fis1 (P<0.05), and a significant reduction in the expression of the mitochondrial outer membrane protein Tom20 and the mitochondrial inner membrane protein Tim23 (P<0.05). Compared with the HIBD group, the 3MA group had a significantly greater reduction in mitochondrial membrane potential (P<0.05), but showed significantly reduced mitophagy (P<0.05). In addition, the 3MA group had a significantly increased degree of cerebral infarction compared with the HIBD group (P<0.05).
conclusionsHIBD can increase the degree of mitophagy, and the inhibition of mitophagy can aggravate HIBD in neonatal rats.
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Identifiers
28202127PMC7389474W2983853413What OpenQuestion holds
Registered trials
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