Emerging evidence has shown that long noncoding RNA (lncRNA) plays a crucial role in controlling neural stem cells' (NSCs) survival. However, the fundamental role of lncRNA underlying sevoflurane-induced neurotoxicity remains poorly elucidated. In the present study, we investigate the effect of sevoflurane-induced neurotoxicity in a concentration-dependent and duration-dependent manner. Furthermore, we assayed the differential profile of lncRNA in rat hippocampal NSCs following sevoflurane exposure, and identified lncRNA Gadd45a and the correlation between lncRNA Gadd45a and Gadd45a. We found that lncRNA Gadd45a and its nearby gene, Gadd45a, were significantly upregulated in NSCs exposed to sevoflurane. Notably, Gadd45a was enriched in the cell cycle-relative pathway including mitogen-activated protein kinases and P53 signaling, whereas lncRNA Gadd45a was positively correlated with Gadd45a. These results suggest lncRNA Gadd45a is associated with sevoflurane-induced toxicity, and thus shed light on a new key target for revealing the molecular mechanism of sevoflurane-induced toxicity.

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Background. Sevoflurane is commonly used as a general anesthetic in neonates to aged patients. Preconditioning or postconditioning with sevoflurane protects neurons from excitotoxic injury. Conversely, sevoflurane exposure induces neurotoxicity during early or late life. However, little is known about the underlying mechanism of the dual effect of sevoflurane on neurons. Autophagy is believed to control neuronal homeostasis. We hypothesized that autophagy determined the dual effect of sevoflurane on neurons. Methods. DTome was used to identify the direct protein target (DPT) of sevoflurane. The STRING database was employed to investigate the proteins associated with the DPTs. Protein-protein interaction was assessed using Cytoscape. WebGestalt was used to analyze gene set enrichment. The linkage between candidate genes and autophagy was identified using GeneCards. Results. This study found that 23 essential DPTs of sevoflurane interacted with 77 proteins from the STRING database. GABARAPL1 and 2, both of which are DPT- and autophagy-associated proteins, were significantly expressed in the brain and enriched in GABAergic synapses. Conclusions. Taken together, our findings showed that the network of sevoflurane-DPT-GABARAPL1 and 2 is related to the dual effect of sevoflurane on neurons.

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Background: The diagnosis of neonatal sepsis remains a challenge as the condition lacks early clinical signs and reliable biomarkers. Objectives: The aim of our study was to determine whether serum mannose binding lectin (MBL) levels and genotypes of MBL2 gene could be used as markers for predicting neonatal sepsis in the Chinese Han population. Methods: This prospective study was hospital-based in design. 48 neonates with clinical signs and symptoms of septicemia (study group), and 96 infants with no infection (control) were included. All the neonates are Chinese Han descent. MBL2 promoter polymorphisms at positions -550, -221 and +4 were analyzed by direct sequencing, and serum MBL levels were estimated by enzyme-linked immunesorbent assay. Results: Frequencies of genotype -221 YX were significantly higher in the study group (45.8%) compared with the control group (15.60%; P = 0.00009). The median serum MBL level was found to be significantly lower in infants who had the -221YX genotype (214.54 ng/mL) compared with those who had the -221YY genotype (597.85 ng/mL; P < 0.0001). Additionally, the median of serum MBL was significantly lower in infants with septicemia (289.65 ng/mL) than in controls (597.75 ng/mL; P = 0.041). According to ROC