Objective To investigate the effects of melatonin on choline acetyltransferase (ChAT) in the hippocampus of rats after isoflurane anesthesia.Methods Sixty male SD rats weighing 390-440 g were randomized into five groups (n =12 each):control group (group C),1％ isoflurane group (group Ⅰ),1％ isoflurane + melatonin group (group IM),2％ isoflurane group (group J) and 2％ isoflurane + melatonin group (group JM).Rats in groups IM and JM received intraperitoneal injection of melatonin (10 mg/kg) for 7 days,and rats in other groups received normal saline.On the 7th day of injection,rats in groups Ⅰ and IM inhaled 1％ isoflurane for 4 hours,and rats in groups J and JM inhaled 2％ isoflurane for 4 hours.One day after anesthesia,all the rats began Morris water maze to assess the learning and memory ability,which was made for continuous 5 days.At the end of probe test,6 rats in each group were randomly selected,blood samples were collected to detect plasma melatonin level,and the hippocampi were removed to evaluate the expression and activity of ChAT.The other rats were sacrificed to perform immunofluorescence to detect ChAT in hippocampal CA1 region and dentate gyrus.Results The plasma melatonin level,and the expression and activity of ChAT were significantly lower in group Ⅰ than in group C (P ＜ 0.01).The escape latency was significantly longer,the probe time was significantly shorter,and the plasma melatonin level and the expression and activity of ChAT were significantly lower in group J than in group C (P ＜ 0.05 or 0.01).The escape latency was significantly shorter,the probe time was significantly longer,and the plasma melatonin level and the expression and activity of ChAT were significantly higher in group IM than in group Ⅰ (P ＜ 0.05 or 0.01).The escape latency was significantly shorter,and the plasma melatonin level and the ChAT activity were significantly higher in group JM than in group J (P＜ 0.05 or 0.01).Conclusion Melatonin can attenuate isoflurane-induced ChAT inhibition and thus improve the cognitive function of rats after isoflurane anesthesia.

Objective: To understand the energy and major nutrients intake of high school students in Shanghai, and to provide basis for formulating target nutritional interventions and health education. Methods: The probability-proportional-to-size sampling technique was used to select 19 high schools, from which 9 boys and 9 girls from same class were randomly recruited for each grade. A total of 900 high school students were surveyed on their energy and major nutrients intake. Results: The medians of intake of energy, protein, fat, carbohydrate, calcium, sodium, iron, vitamin A, vitamin B-1, vitamin B-2, vitamin C and dietary fiber were 2 353 kcal/d, 97.3 g/d, 95.4 g/d, 265.4 g/d, 602.1 mg/d, 4 373 mg/d, 24.3 mg/d, 495.6 μgRE/d, 1.08 mg/d,1.21 mg/d, 83.2 mg/d and 1.01 g/d, respectively. Among of them, the medians of intake of energy, calcium, vitamin A, vitamin B-1, vitamin B-2, vitamin C and dietary fiber for boys and girls were lower than reference standard(P<0.05). The medians of intake of energy and major nutrients in high school students who lived in countryside were less than those lived in suburban and urban(P<0.05), except carbohydrates and iron. The percentages of energy supplied byprotein, fat and carbohydrate were 16.9%, 37.2%and 46.0%, respectively. Conclusion The energy and calorigenic nutrients intake can meet the demand of daily consumption in high school students in Shanghai, but the intake of dietary fiber, some minerals and vitamins have a various degrees of deficiency. The proportion of energy supplied bycalorigenic nutrients is unbalanced.

Objective:To investigate the effects and mechanism of cannabinoid (CBD) on the anxiety- and depression-like behaviors induced by lipopolysaccharide (LPS) in mice.Methods:C57BL/6J mice were intraperitoneally injected with LPS to establish the model of neuroinflammation. CBD was injected intraperitoneally 24 h after modeling. Behavioral tests were performed to evaluate the anxiety- and depression-like behaviors in mice. CBD-pretreated BV-2 microglia cells were stimulated with LPS in vitro. The levels of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and CD86 in mouse cerebral cortex, hippocampus, prefrontal cortex and BV-2 cells were measured by qRT-PCR. The protein level of nuclear factor (NF-κB) in mouse brain and BV-2 cells was determined by Western blot. Results:CBD significantly increased the residence time and movement distance of LPS-treated mice in the central area in the open filed test (OFT), and reduced the immobility time in tail suspension test (TST) and force swimming test (FST). In addition, CBD alleviated the neuroinflammation and inhibited the activation of microglia in mouse brain. In vitro, CBD significantly inhibited the activation of BV-2 microglia cells. Both in vivo and in vitro experiments confirmed that CBD could inhibit NF-κB expression. Conclusions:LPS could induce the activation of BV-2 microglia cells and the expression of inflammatory factors in mouse brain accompanied with abnormal behaviors. CBD could inhibit the activation of microglia, alleviate the neuroinflammation in different regions of mouse brain and improve behavioral performance.