Long noncoding RNA (lncRNA) is a kind of RNA with a length greater than 200 nucleotides and lacks protein-coding function.Varieties of lncRNAs have been found to play major roles in the aerobic glycolysis of tumor cells,such as lncRNA-p21,H19,prostate specific transcript 1 (PGCEM1) and so on.In tumor cells,lncRNA can directly regulate the rate-limiting enzyme in the glycolytic pathway,also can indirectly regulate the glycolysis by hypoxia inducible factor-1α (HIF-1α) or proto-oncogene c-myc.Further study on the mechanism of lncRNA regulating tumor cell glycolysis is expected to open up new ideas for the diagnosis and treatment of tumor diseases.

Objective:To evaluate the role of sonic hedgehog (Shh)/glioma-associated oncogene homolog 1 (Gli1) signaling pathway in sleep deprivation-induced cognitive impairment in young mice.Methods:Forty-eight SPF healthy male C57BL/6 mice, aged 4 weeks, weighing 14-16 g, were divided into 3 groups ( n=16 each) by the random number table method: control group (C group), sleep deprivation group (SD group) and Shh agonist SAG group (SD+ SAG group). Multi-platform water environment method was used to prepare the sleep deprivation model in mice, and the sleep deprivation was 20 h a day for 10 consecutive days.In SD+ SAG group, SAG 10 mg/kg was intraperitoneally injected at 5 min before each sleep deprivation, while the equal volume of normal saline was intraperitoneally injected in group C and group SD.The mice underwent novel object recognition and Y-maze tests at 24 h after development of the model.Mice were sacrificed after the behavioral testing, and the hippocampi were isolated for determination of the density of dendritic spines in hippocampal CA1 region (by Golgi staining), expression of Gli1 and brain-derived neurotrophic factor (BDNF) in hippocampal tissues (by Western blot), and expression of Gli1 and BDNF mRNA in hippocampal tissues (by quantitative real-time polymerase chain reaction). Results:Compared with group C, the preference index in novel object recognition and Y-maze tests and density of dendritic spines in CA1 region were significantly decreased, and the expression of Gli1 and BDNF protein and mRNA in hippocampus was down-regulated in group SD ( P<0.05). Compared with group SD, the preference index in novel object recognition and Y-maze tests and density of dendritic spines in CA1 region were significantly increased, and the expression of Gli1 and BDNF protein and mRNA in hippocampus was up-regulated in group SD+ SAG ( P<0.05). Conclusions:Inhibition of Shh/Gli1 signaling pathway and reduction of plasticity of dendritic spines of hippocampal neurons are involved in sleep deprivation-induced cognitive impairment in young mice.

Objective:To evaluate the effect of sleep deprivation on the expression of sirtuin 6 (SIRT6) in the cerebellum of immature mice.Methods:Fifty SPF healthy male C57BL/6 mice, aged 4 weeks, weighing 14-16 g, were divided into 2 groups ( n=25 each) using a random number table method: control group (Con group) and sleep deprivation group (SD group). The chronic sleep deprivation model was prepared by using the multi-platform water environment method, with 20 h of sleep deprivation per day for 10 consecutive days. After sleep deprivation, a balance beam experiment was performed to test the balance and coordination ability of mice. The mice were sacrificed after anesthesia and cerebellar lobular IV-VI (4-6 cb) tissues were taken for microscopic examination of the ultrastructure (with a transmission electron microscope) and for determination of the dendritic spine density of cerebellar 4-6cb Purkinje neurons (by Golgi staining), co-expression of SIRT6 and Calbindin D-28k (CbD-28k) and expression of glucose transporter Glut3 of cerebellar 4-6cb (by immunofluorescence staining). Results:Compared with group Con, the duration of passage through the balance beam was significantly prolonged, and the number of posterior foot slips was increased, the synaptic gap of cerebellar 4-6cb neurons was increased, the thickness of postsynaptic density was increased, the density of dendritic spines of Purkinje cells and the number of positive cells co-expressing SIRT6 and CbD-28k were decreased, and the expression of Glut3 was down-regulated in group SD ( P<0.05). Conclusions:The mechanism by which sleep deprivation decreases the abilities of balance and coordination is related to down-regulating SIRT6 expression in cerebellar Purkinje cells and decreasing neuronal glucose metabolism, thus damaging the synaptic plasticity of cerebellum in immature mice.