Autophagy is involved in sevoflurane-induced developmental neurotoxicity in the developing rat brain.

BACKGROUND

Sevoflurane can induce neonatal wide neurodegenerative and serious deficit to space learning tasks in rodents, however, the specific mechanism is still unclear. At present, the study tried to explore the possible role of autophagy in sevoflurane-induced neurotoxicity through observing the changes in the levels of autophagy in the newborn SD rat hippocampus tissue after sevoflurane exposure.

METHODS

We used seventy-two SD rats of seven days receiving sevoflurane exposure to explore hippocampus neuron autophagy and apoptosis.

RESULTS

Our results indicated that sevoflurane increased the levels of Beclin-1, microtubule-associated protein light chain 3II protein and decreased sequestosome 1 levels in a time-dependent manner by Western blot in the developing brain. These results were further substantiated by transmission electron microscopy, quantitative reverse transcription polymerase chain reaction, immunohistochemistry and immunofluorescence. Rapamycin, an activator of autophagy, increased the levels of Beclin-1and LC3-II protein, meanwhile, 3-methyladenine, an inhibitor of autophagy, decreased Beclin-1and LC3-II protein levels.

CONCLUSION

Taken together, autophagy may be involved in sevoflurane-induced developmental neurotoxicity and promoting protective autophagy may be a potential way of preventing developmental sevoflurane-induced neurotoxicity.