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<p>Sevoflurane is an inhalation anesthetic in pediatric anesthesia which may cause cognitive dysfunction. Our study explores the mechanisms of fat mass and obesity-associated protein (FTO) in sevoflurane-induced cognitive impairment in neonatal rats. A neonatal rat model was established by 3% sevoflurane exposure. After FTO or miR-188-5p overexpression in rats, the motor and cognitive function and hippocampal tissue were tested. A cell model was established by 3% sevoflurane exposure in hippocampal neuronal cells. After FTO overexpression, cell viability, apoptosis, and lactate dehydrogenase levels were detected. The enrichment of m6A on the pri-miR-188 was analyzed. The binding of miR-188-5p to the SRY-box transcription factor 4 (SOX4) 3’UTR sequence was detected. <b>S</b>evoflurane exposure triggered cognitive impairment in neonatal rats and decreased FTO expression in hippocampus. FTO upregulation reduced cognitive impairment in neonatal rats and hippocampal neuronal cell damage in vitro. In hippocampus and cell models, FTO inhibited miR-188-5p expression by removing m6A modification on pri-miR-188. miR-188-5p inhibited SOX4 expression. miR-188-5p overexpression or SOX4 inhibition partially reversed the protective effects of FTO overexpression on hippocampal neuronal cell damage. Overexpression of miR-188-5p partially reversed the alleviative effects of FTO overexpression on cognitive impairment. In conclusion, FTO attenuates cognitive impairment in neonatal rats through the miR-188-5p/SOX4 axis via m6A modification.</p>

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Mechanisms of Fat Mass and Obesity-Associated Protein in Regulating Cognitive Impairment Induced by Sevoflurane Anesthesia in Neonatal Rats

  • 期刊论文

  • 发表日期：

    2025年5月30日

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  • Chan Shen,
  • Yanghongyun Guo,
  • Jun Zheng,
  • Jiayu Wang,
  • Liangcheng Zhang

摘要

Sevoflurane is an inhalation anesthetic in pediatric anesthesia which may cause cognitive dysfunction. Our study explores the mechanisms of fat mass and obesity-associated protein (FTO) in sevoflurane-induced cognitive impairment in neonatal rats. A neonatal rat model was established by 3% sevoflurane exposure. After FTO or miR-188-5p overexpression in rats, the motor and cognitive function and hippocampal tissue were tested. A cell model was established by 3% sevoflurane exposure in hippocampal neuronal cells. After FTO overexpression, cell viability, apoptosis, and lactate dehydrogenase levels were detected. The enrichment of m6A on the pri-miR-188 was analyzed. The binding of miR-188-5p to the SRY-box transcription factor 4 (SOX4) 3’UTR sequence was detected. Sevoflurane exposure triggered cognitive impairment in neonatal rats and decreased FTO expression in hippocampus. FTO upregulation reduced cognitive impairment in neonatal rats and hippocampal neuronal cell damage in vitro. In hippocampus and cell models, FTO inhibited miR-188-5p expression by removing m6A modification on pri-miR-188. miR-188-5p inhibited SOX4 expression. miR-188-5p overexpression or SOX4 inhibition partially reversed the protective effects of FTO overexpression on hippocampal neuronal cell damage. Overexpression of miR-188-5p partially reversed the alleviative effects of FTO overexpression on cognitive impairment. In conclusion, FTO attenuates cognitive impairment in neonatal rats through the miR-188-5p/SOX4 axis via m6A modification.