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<p>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&#xa0;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&#xa0;h post-HI, concurrent with increased BNIP3 and RIP3 expression, and elevated apoptosis and necroptosis, at both 24 and 48&#xa0;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.</p>

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miRNA-105 Attenuates Hypoxic-Ischemic Brain Damage in Neonatal Rats by Inhibiting Apoptosis and Necroptosis

  • 期刊论文

  • 发表日期：

    2025年7月21日

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  • Junyan Liu,
  • Hui Li,
  • Yi Qu,
  • Shiping Li,
  • Fengyan Zhao

摘要

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.