Journal
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume 52, Issue -, Pages 121-128Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.etap.2017.03.017
Keywords
Propofol; Dexmedetomidine; Apoptosis; AKT; GSK3 beta
Funding
- National Natural Science Foundation of China [81373498, 81060277]
- Science Study and Technology Development Program of Guangxi [1355005-4-2]
- Science and Technology Research Project of Guangxi University [2013ZD014]
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Recent studies have demonstrated that propofol causes neurodegeneration in developing brains. Evidence has shown that dexmedetomidine has neuroprotective effects. However, whether dexmedetomidine can reduce propofol-induced neuroapoptosis and by what mechanisms it acts remain unclear. We investigated whether dexmedetomidine can attenuate propofol-induced neuroapoptosis by disturbing the PI3K/Akt/GSK3 beta pathway during brain development. Seven-day-old rats were randomly exposed to 100 mg/kg propofol and 100 mg/kg propofol plus different doses of dexmedetomidine or 100 mg/kg propofol and 75 g/kg dexmedetomidine plus PI3K inhibitor LY294002 or GSK3 beta inhibitor TDZD-8. TEM and TUNEL were used to detect neuronal structure changes and apoptosis. The expression of phospho-Akt, phospho-GSK3 beta, Akt and GSK3 beta were quantified using western blots and immunofluorescence. Pretreatment with different doses of dexmedetomidine protected against propofol-induced neuroapoptosis. Furthermore, propofol decreased the levels of phospho-Akt and phosphoGSK313, whereas dexmedetomidine partially reversed this inhibition. In addition, treatment with LY294002 inhibited the neuroprotection of dexmedetomidine, whereas TDZD-8 enhanced neuroprotection. Our results indicate that dexmedetomidine prevents propofol-induced neuroapoptosis by increasing the levels of phosphoAkt and phospho-GSK3 beta.
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