ArticleNeurochemical research2025
miRNA-105 Attenuates Hypoxic-Ischemic Brain Damage in Neonatal Rats by Inhibiting Apoptosis and Necroptosis.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Integrated analysis of porcine brain microRNA profiles following pediatric diffuse traumatic brain injury.Acta neuropathologica communications · 2026Article
- The Potential Clinical Relevance of Necrosis-Necroptosis Pathways for Hypoxic-Ischaemic Encephalopathy.Cells · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
Apoptosis and necroptosis contribute significantly to cell death in hypoxic-ischemic encephalopathy (HIE). While microRNA-105 (miR-105) is known to suppress both apoptosis and necroptosis in cardiac ischemia, its role in HIE remains unclear. This study investigated the effects of miR-105 on apoptosis and necroptosis in a neonatal rat model of HIE. MiR-105 agomir was administered intracerebroventricularly 6 h post-hypoxic-ischemia (HI). The characteristic apoptosis-related proteins (BNIP3, cleaved caspase 3), necroptosis mediators (RIP3, p-RIP3, p-RIP1, p-MLKL), cerebral infarction, and neurological deficits were analyzed. Results showed miR-105 was significantly downregulated in cerebral cortex from 6 to 48 h post-HI, concurrent with increased BNIP3 and RIP3 expression, and elevated apoptosis and necroptosis, at both 24 and 48 h. MiR-105 agomir treatment suppressed BNIP3 and RIP3 expression, reduced apoptosis and necroptosis, attenuated infarct volume, lowered neurological severity score, and improved spatial learning and memory abilities. In conclusion, miR-105 alleviates HI brain injury in neonatal rats by simultaneously inhibiting apoptosis and necroptosis, highlighting its potential as therapeutic agent for HIE.
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Registered trials
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