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Purpose <p>Hypoxia may occur during general anesthesia and is associated with cerebral ischemia and postoperative cognitive decline. Although intranasal insulin (INI) can alleviate mild hypoxic cerebral injury, its potential for therapeutic application remains underexplored. In this study, we aimed to investigate the effects and changes in INI-induced gene expression in mouse models of cerebral hypoxic-ischemic injury.</p> Methods <p>Brain injury was induced in 8–10-week-old male C57BL/6 mice via a combination of left common carotid artery ligation and exposure to 8% oxygen for 15&#xa0;min. The mice were allocated to an INI or control group (<i>n</i> = 8 in each group), receiving either 1.7 IU (17 µL) of insulin or saline intranasally. Infarct volume and neurological deficit scores (NDS) were also assessed. RNA sequencing was performed to identify potential genes and the signaling pathways involved.</p> Results <p>Cerebral infarction volumes did not differ between the two groups. NDS at 1 and 2 days following ischemic insult was lower in the INI group. However, no significant differences were observed after that. RNA sequencing analysis showed that the <i>Oxt</i> gene and neuronal pathways were upregulated in the INI group.</p> Conclusion <p>INI improved behavioral symptoms temporarily, although cerebral infarct volume remained unchanged. As a possibility, the effects might be related to the <i>Oxt</i> gene expression.</p>

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Intranasal Insulin Transiently Improves Early Neurological Deficits and Alters Oxytocin-Related Gene Expression After Mild Hypoxic-Ischemic Brain Injury in Mice

  • 期刊论文

  • 发表日期：

    2025年10月29日

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  • Takuya Akiyama,
  • Yosuke Nakadate,
  • Kodai Ikemoto,
  • Sohei Hishiyama,
  • Kazuha Mitsui,
  • Masakazu Kotoda,
  • Masako Abe,
  • Takashi Matsukawa

摘要

Purpose

Hypoxia may occur during general anesthesia and is associated with cerebral ischemia and postoperative cognitive decline. Although intranasal insulin (INI) can alleviate mild hypoxic cerebral injury, its potential for therapeutic application remains underexplored. In this study, we aimed to investigate the effects and changes in INI-induced gene expression in mouse models of cerebral hypoxic-ischemic injury.

Methods

Brain injury was induced in 8–10-week-old male C57BL/6 mice via a combination of left common carotid artery ligation and exposure to 8% oxygen for 15 min. The mice were allocated to an INI or control group (n = 8 in each group), receiving either 1.7 IU (17 µL) of insulin or saline intranasally. Infarct volume and neurological deficit scores (NDS) were also assessed. RNA sequencing was performed to identify potential genes and the signaling pathways involved.

Results

Cerebral infarction volumes did not differ between the two groups. NDS at 1 and 2 days following ischemic insult was lower in the INI group. However, no significant differences were observed after that. RNA sequencing analysis showed that the Oxt gene and neuronal pathways were upregulated in the INI group.

Conclusion

INI improved behavioral symptoms temporarily, although cerebral infarct volume remained unchanged. As a possibility, the effects might be related to the Oxt gene expression.