AI Article Synopsis

  • A study investigated the effect of 3-methyladenine (3-MA) on cognitive dysfunction caused by sevoflurane anesthesia in mice.
  • Sevoflurane led to significant cognitive impairment, as evidenced by longer escape latencies and increased neuronal apoptosis in the Morris water maze and Y-maze tests.
  • The addition of 3-MA during sevoflurane exposure mitigated cognitive deficits, suggesting its potential as an inhibitor of anesthesia-induced cognitive dysfunction for future clinical use.

Article Abstract

This study was designed to explore the effect of 3-methyladenine (3-MA) on sevoflurane anesthesia-induced cognitive dysfunction. A total of 60 C57BL/6 (5-8 months old) mice were randomly arranged into 3 groups: Control, sevoflurane (Sev) and Sev+3-MA group with 3-MA administration was performed during Sev administration. Morris water maze and Y-maze test were performed to examine the behavioral disorders. Moreover, hippocampal neuronal cell apoptosis and expression of autophagy related genes were detected. Sevoflurane induced cognitive dysfunction in mice showing significant longer escape latency, lower number of correct response, higher apoptotic neurons, and higher expression of autophagy related genes. However, additional 3-MA administration inhibited the effect of sevoflurane on cognitive dysfunction by shorting escape latency, reducing correct response number, inhibiting neurons apoptosis and autophagy genes expression. 3-MA additional administration inhibited sevoflurane anesthesia-induced cognitive dysfunction on mice. 3-MA might be usefull as an inhibitor for sevoflurane anesthesia-induced cognitive dysfunction in clinical trials.

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Source
http://dx.doi.org/10.1691/ph.2017.6872DOI Listing

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