Abstract: Objective · To investigate the role of long non-coding RNA (lncRNA) Peg13 (paternally expressed 13) in the apoptosis of developing primary neurons following sevoflurane injury. Methods · Primary neurons were prepared fetal mice with 14.5 d of gestational age. The of lncRNA Peg13 after sevoflurane treatment was detectedquantitative PCR. The localization of lncRNA Peg13 in primary neurons was detectedin situ hybridization. Peg13 over and knockdown plasmids were constructed and transfected into primary neurons. The morphology of primary neurons was observedfluorescence microscope. Cell vability was assessedCCK-8 assay. Cell apoptosis was determinedTUNEL assay and Western blotting. Results · The of lncRNA Peg13 in primary neurons decreased in a time-dependent manner after sevoflurane treatment. LncRNA Peg13 was widely expressed in the cytoplasm and axon of primary neuron. Over of lncRNA Peg13 resulted in decreased sevoflurane-induced apoptosis. The primary neurons were restored to normal morphology with increased cell vability. The percentage of TUNEL-positive cells was decreased. The ratio of Bcl-2/Bax was increased and the of casepase-3 was decreased. However, knockdown of lncRNA Peg13 aggravated the sevoflurane-induced apoptosis. The primary neurons had visible morphological deterioration and decreased cell vability, with increased percentage of TUNEL-positive cells, decreased ratio of Bcl-2/Bax, and increased of casepase-3. Conclusion · LncRNA Peg13 may alleviate sevofluraneinduced apoptosis in developing primary neurons.

Key words: sevoflurane, long non-coding RNA Peg13, developing primary neuron, cell vability, apoptosis