Objective To investigate the role of long non-coding RNA-small nucleolar RNA host gene 3(lncRNA-Snhg3)and its regulatory mechanism in the hepatic glucose metabolism of mice.Methods Adenovirus Snhg3 was over-expressed by the tail vein injection in db/db mice,and then glucose tolerance and pyruvate tolerance were meas-ured.The mRNA expression of mouse liver gluconeogenesis-related genes phosphoenolpyruvate carboxylase(Pepck)and glucose-6-phosphatase(G6pc)and stress-inducing protein 2(Sestrin2,Sesn2,a gene adjacent to Snhg3)were de-tected by RT-qPCR.The dual luciferase reporter assay was used to detect the effect of Snhg3 on the Sesn2 promoter activity in 293T cells.Results Snhg3 over-expression improved glucose tolerance and pyruvate tolerance in db/db mice.Snhg3 over-expression inhibited the mRNA of gluconeogenesis genes of Pepck(P＜0.05)and G6pc(P＜0.05),while promoted the mRNA of Sesn2(P＜0.01).Meanwhile,Snhg3 over-expression promoted Sesn2 promoter activity in 293T cells(P＜0.05).Conclusions Snhg3 improves glucose metabolism in mice by promoting Sestrin2 expression.

BACKGROUND:Drug therapy can partly reduce and delay the progress of Alzheimer’s disease, but only 30%with the single drug treatment obtain clinical cure. OBJECTIVE:To study the therapeutic effect of bone marrow mesenchymal stem cel s transplantation for rats with Alzheimer’s disease. METHODS:Amyloidβ-protein was injected into the hippocampus of Sprague-Dawley rats to construct the model of Alzheimer’s disease. And bone marrow stromal stem cel s were transplanted into the hippocampus of the rat models. RESULTS AND CONCLUSION:At 2 weeks after modeling, compared with the control group, the escape latency in the model and experimental groups was significantly longer (P<0.05), which indicating that Alzheimer’s disease models were successful y established. At 4 weeks after cel transplantation, compared with the model group, the average escape latency in the experimental group was significantly decreased, but retention time on the platform quadrant was significantly prolonged (P<0.05). Besides, at 4 weeks after cel transplantation, expression of choline acetyltransferase in the experimental group was significantly higher than that in the model group (P<0.05). In conclusion, bone marrow mesenchymal stem cel s cannot only differentiate and survive in the hippocampus of rats with Alzheimer’s disease, but also improve the learning and memory ability.

BACKGROUND:Drug treatment for senile dementia has unsatisfactory outcomes although to a certain extent it can reduce and delay the progression of Alzheimer’s disease. Stem cel transplantation is a new attempt for the treatment of senile dementia.
OBJECTIVE:To observe the effect of bone marrow mesenchymal stem cel transplantation on the behavior of senile dementia rats.
METHODS: Rat models of senile dementia were made in 20 Sprague-Dawley rats that were given continuous 60-day gavage of aluminium chloride solution. Then, model rats were randomized into model group treated with normal saline injection and experimental group treated with hippocampal injection of bone marrow mesenchymal stem cels, respectively. Another 10 rats undergoing normal feeding served as control group. Learning and memory ability of rats were tested by Morris water maze, and superoxide dismutase activity and malondialdehyde content in brain tissues of rats were measured by colorimetric method at 4 weeks after cel transplantation.
RESULTS AND CONCLUSION:Compared with the model group, the escape latency was shortened and the cross-platform frequency was increased in the experimental group (P < 0.05), and moreover, significantly elevated superoxide dismutase activity and reduced malondialdehyde content in the brain tissues of rats were found in the experimental group (P < 0.05). These findings indicate that bone marrow mesenchymal stem cel transplantation contributes to behavior improvement in senile dementia rats by improving the learning and memory ability.

Objective To determine the optimal dose range of naloxone to enhance the analgesic effect of morphine.Methods One half of a total of 84 adult male Sprague-Dawley rats were randomly assigned into seven groups(6 rats for each group).Rats in group NS received normal saline,and in group M received 6mg/kg of morphine.Different doses of naloxone(1?g/kg,100ng/kg,10ng/kg,1ng/kg and 0.1ng/kg)with 6mg/kg of morphine were given to the rats in group MN1,group MN2,group MN3,group MN4 and group MN5.Pain thresholds were determined at different time points before and after subcutaneous injection of normal saline or morphine or mixture of the drugs(morphine and naloxone).Another 42 rats were randomly assigned into seven groups similar to the above grouping,but the morphine doses for group M and groups MN were changed to 2mg/kg.Acute pain was prodused by an in cision on the hind paw.Then they were given subcutaneous injection of the drugs in different doses as categorized above.Cumulative pain scores were observed within an hour.Results Compared with group NS,the pain thresholds of all the other groups were significantly increased at the time points from 5 minutes to 120 minutes after subcutaneous injection(P0.05).Conclusions Low-dose of naloxone can enhance the analgesic effect of morphine,and the dose range 1ng/kg~100ng/kg may be acceptable.Dose of 1?g/kg naloxone may antagonize the analgesic effect of morphine,while dose of 0.1ng/kg naloxone,perhaps,is too low to show an effect.