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 from fetal mice with 14.5 d of gestational age. The expression of lncRNA Peg13 after sevoflurane treatment was detected by quantitative PCR. The localization of lncRNA Peg13 in primary neurons was detected by in situ hybridization. Peg13 overexpression and knockdown plasmids were constructed and transfected into primary neurons. The morphology of primary neurons was observed by fluorescence microscope. Cell vability was assessed by CCK-8 assay. Cell apoptosis was determined by TUNEL assay and Western blotting. Results • The expression 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. Overexpression 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 expression ratio of Bcl-2/Bax was increased and the expression 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 expression of casepase-3. Conclusion • LncRNA Peg13 may alleviate sevoflurane-induced apoptosis in developing primary neurons.