Objective: To explore the role of Neurotropfin-3 (NT-3) in hypoxic-ischemic encephalopathy (HIE) and determine its relative molecular mechanism. Methods: The expression of NT-3 was determined by qRT-PCR in the cortex after HIE and immunoluorescence staining was used to detect the distribution of NT-3. Then, the NT-3 siRNA was used to validate the efect of NT-3 for the neuroprotection by the measurement of cell apoptosis after oxygen-glucose deprivation (OGD). Lastly, the molecular network mechanism was studied by NT-3 interference experiment combined with bioinformatics technology. Results:The expression of NT-3 was signiicantly upregulated after HIE, and NT-3 was co-localized in the neurons of the cortex. Furthermore, the inhibition of NT-3 increased neuronal apoptosis after OGD and elicited the down-regulation of BDNF and NGF. Conclusion:NT-3 is a vital neurotrophic factor that can maintain neonatal survival in cortical neurons, and the underlying mechanism is associated with BDNF and NGF regulation.

Optimal exercise can promote the development of cognitive functions. Nevertheless, mechanisms that elicit these positive effects of exercise still need to be elucidated. Insulin-like growth factor 2 (IGF2) is known to act as a potent enhancer of memory and cognitive functions, whereas the mechanism by which IGF2 regulates cognitive functions in terms of moderate treadmill exercise remains largely vague. In the study, rats were subjected to low-, moderate-, and high-intensity treadmill training for 6 weeks. Then, the Morris water maze test was used to investigate spatial learning and memory ability in rats subjected to treadmill exercises of different intensities. Subsequently, gene chip and bioinformatics analyses were used to explore IGF2 and predict target microRNAs (miRNAs). Quantitative real-time polymerase chain reaction, western blot, and immunofluorescence analysis were performed to detect the levels of IGF2. Furthermore, IGF2-small interfering RNA, the miRNA-483mimic, and the miRNA-483-inhibitor were transfected to determine the role of IGF2 and miRNA-483 in the growth of hippocampal neurons. The results of the Morris water maze test showed that moderate-intensity treadmill training enhanced cognitive functions; meanwhile, the expression of IGF2 was significantly upregulated in the hippocampus after moderate-intensity treadmill exercise. From databases, miRNA-483 was screened and predicted as the target gene of IGF2. Moreover, silencing IGF2 inhibited neurite growth in the hippocampus of rats, the miRNA-483-inhibitor ameliorated silencing IGF2 induced impairment of hippocampal neurons. These findings suggested that treadmill training could enhance cognitive functions, wherein the underlying mechanism involved an increase in the expression of IGF2 and downregulation of miRNA-483.

This study aimed to explore whether the combined application of desflurane and dexmedetomidine (Dex) reduces the occurrence of postoperative neurocognitive disturbance (PND) in patients. We selected patients in our hospital who underwent surgery under general anesthesia, and divided them into two groups: Dex and desflurane (Dex + Des) and desflurane (Des) groups. The data of patients were collected and the Mini‐Mental State Examination (MMSE) score was used to assess cognitive status. The blood cell counts were determined preoperatively and on postoperative days 1, 3, and 6, and the percentage of neutrophils and lymphocytes were also recorded. The statistical methods used were the independent‐samples t‐test and the χ2 test. Pearson's correlation was used to analyze the correlation between PND and inflammation. The incidence of PND in the Dex + Des group was lower than that in the Des group. The postoperative MMSE scores in the Dex + Des group were higher than those in the Des group (p = 0.032). The percentage of neutrophils in the Dex + Des group was significantly lower than that in the Des group on the first and third days after surgery (p = 0.007; p = 0.028). The MMSE scores on the first day after surgery were negatively correlated with the multiple changes in white blood counts and the percentage of neutrophils (r = −0.3038 and −0.3330). Dex combined with Des reduced the incidence of PND and reduced the postoperative inflammatory cell counts.

Objects: Explore the relationship between the neural function deicit and the changes of lncRNA and mRNA in hippocampus after traumatic brain injury (TBI) in rats.Methods: Twenty male rats weighted 200-240 grams were randomly divided into sham group and TBI group. Neurologic severity score (NSS) was performed after operation, and the hippocampus of rats was collected for long non-coding RNAs (lncRNAs), mRNAs microarray detection, real-time quantitative PCR Detecting System (Q-PCR), western blot (WB) detection, and serum biochemical detection. Results:The NSS score of the TBI group was signiicantly higher than the sham group. Compared with the sham group, 270 lncRNAs changed in the TBI group, of which 224 were up-regulated and 46 were down-regulated. Among up-regulated lncRNAs, mRNAs were distributed in upstream of 22 lncRNAs, downstream of 17 lncRNAs, overlapping regions of 48 lncRNAs, and antisense chains of 21 lncRNAs. Among down-regulated lncRNAs, mRNAs were distributed in upstream of 6 lncRNAs, downstream of 3 lncRNAs, overlapping regions of 10 lncRNAs, and antisense chains of 8 lncRNAs. Compared with the sham group, 1054 mRNA changed in the TBI group, of which 921 mRNA were up-regulated and 133 mRNA were down-regulated. The expression changes of ENSRNOT000063054, ENSRNOT000052790, ENSRNOT00000054410, ENSRNOT000063242, and ENSRNOT000069411 IncRNA regulate the expression of Top2a, RT1-CE11, Papss2, Stk32a, and Grid2 gene. Conclusion:The present study detected the differential expression of lncRNAs and mRNAs in hippocampi of rats subjected to TBI, and discussed their relation, primarily.