BACKGROUND: Studies have demonstrated that trehalose possesses protective effects on cyropreserved sternum. But the mechanism of action remains poorly understood. OBJECTIVE: To investigate the effects of trehalose on bcl-2 and bax mRNA expression in cryopreserved sternum. METHODS: Four groups of freshly prepared solution were used: low-potassium dextran (LPD), LPD + dimethyl sulfoxide (DMSO), LPD + trehalose, LPD + DMSO + trehalose. Rat sternum was cut and then immediately cryopreserved in the tubes containing each group of solution. Fresh rat sternum tissue and 4 groups of samples cryopreserved for 120 days were taken and bcl-2 and bax mRNA expression in fresh and cryopreserved sternum was detected using reverse transcription-polymerase chain reaction.RESULTS AND CONCLUSION: bcl-2 mRNA expression in the LPD + trehalose group was significantly higher, but bax mRNA expression was significantly lower, than in the LPD, LPD + DMSO groups (both P < 0.01). LPD + DMSO + trehalose group showed highest bcl-2 mRNA expression and lowest bax mRNA expression, which were basically similar to fresh bone tissue (P > 0.05). These findings indicate that trehalose may protect cell activity in cryopreserved sternum by enhancing bcl-2 mRNA expression and inhibiting bax mRNA expression, and trehalose together with DMSO shows better protective effects.

Alzheimer's disease (AD) is a central neurodegenerative disease with still unclear pathogenesis. Recent studies have shown that axonal transport dysfuction of mitochondria may contribute to AD progression. Normal mitochondrial axonal transport mainly involves microtubules, molecular motors and connexins, while AD early pathological changes can damage mitochondrial axonal transport by interfering with these proteins: accumulated β-amyloid (Aβ) impairs the function of molecular motors; abnormally modified Tau protein reduces microtubule stability; mutant presenilin-1 (PS1) can induce phosphorylation of some related proteins by activating glycogen synthase kinase-3β (GSK-3β); all these processes can damage mitochondrial axonal transport, leading to synaptic dysfunction. This review aims to clarify the possible mechanisms of axonal transport dysfuction of mitochondria in AD and provides new ideas for AD treatment.

Dexmedetomidine,which is an α2 adrenergic receptor agonist with sedative,analgesic,anxiolytic and anti-sympathetic effects,has become a widely used drug in clinical anesthesia and intensive care unit(ICU).Compared with other drugs in the department of anesthesiology,dexmedetomidine has no obvious respiratory depression and no obvious hemodynamic changes,and can significantly reduce the dosage of sedative and analgesic drugs when combined with other anesthetics.In clinical applications,dexmedetomidine has been found to induce a sedative response that is associated with rapid arousal.Dexmedetomidine is traditionally thought to act through α2 adrenergic receptors to lower blood pressure,dilate blood vessels and lower heart rate,but it is unclear how it affects neural circuits in the brain.In recent years,there has been an increasing number of studies on the mechanism of action of dexmedetomidine,which has confirmed that the ventrolateral preoptic nucleus(VLPO),locus coeruleus(LC)and ventral tegmental area(VTA)of the hypothalamus are involved in the sedation mediated by dexmedetomidine,the dorsal root ganglion(DRG)and superior cervical ganglion(SCG)are involved in dexmedetomidine-mediated analgesia,and the hypothalamic preoptic area(PO)and hypothalamic paraventricular nucleus(PVN)are involved in the changes in body temperature and water-electrolyte balance mediated by dexmedetomidine,providing a new direction for understanding the mechanism of dexmedetomidine in the central nervous system.

Microglia (MG) are resident immune cells in the central nervous system (CNS) and the first defense line of CNS damage. The maintenance of MG function requires abundant energy, and lipid can serve as an energy source for the brain when glucose utilization is limited, and lipid can also function as signaling molecule. Alzheimer's disease (AD) is the most common neurodegenerative disease, and MG lipid metabolism plays an important role in the development of this disease. Drugs targeting lipid metabolism provide a new direction for AD treatment. This review starts with the specific mechanism of lipid metabolism in MG, and briefly introduces the effect of lipid metabolism on MG function and its role in AD.

Objective:To discuss the improvement effect of uric acid(UA)on the postoperative cognitive dysfunction(POCD)in the mice anesthetized with isoflurane for a long duration,and to clarify its possible mechanism.Methods:Twenty-four healthy male C57BL/6 mice were randomly divided into blank control group,anesthesia group,and UA group,and there were eight mice in each group.The mice in UA group were injected intraperitoneally with 200 μL UA solution daily for 2 d before anesthesia.The mice in blank control group and anesthesia group were given the same volume of saline;the mice in anesthesia group and UA group were used to prepare the models of long-duration isoflurane anesthesia,while the mice in blank control group were untreated.Y-maze tests was used to detect the alternation success rate,movement distances,and movement speeds of the mice in various groups;situational fear experiment was used to detect the percentages of freezing time;Western blotting method was used to detect the expression levels of interleukin(IL)-1β,IL-10,and mature brain-derived neurotrophic factor(mBDNF)proteins in hippocampus tissue of the mice in various groups.Results:The Y-maze test results showed that compared with blank control group,the alternation success rate of the mice in anesthesia group was significantly decreased(P<0.01);compared with anesthesia group,the alternation success rate of the mice in UA group was significantly increased(P<0.01).The situational fear experiment results showed that compared with blank control group,the percentage of freezing time of the mice in anesthesia group was significantly decreased(P<0.01);compared with anesthesia group,the percentage of freezing time of the mice in UA group was significantly increased(P<0.05).The cued memory experiment resutls showed that there were no significant differences of the percentage of freezing time of the mice between various groups(P>0.05).The Western blotting results showed that compared with blank control group,the expression level of IL-1β protein in hippocampus tissue of the mice in anesthesia group was increased(P<0.01),while the expression levels of IL-10 and mBDNF proteins were decreased(P<0.01);compared with anesthesia group,the expression level of IL-1β protein in hippocampus tissue of the mice in UA group was decreased(P<0.05),and the expression levels of IL-10 and mBDNF proteins were increased(P<0.05 or P<0.01).Conclusion:UA can improve the POCD in the mice,and its mechnasim may be related with its anti-inflammatory activity inhibiting the central inflammation and upregulating the mBDNF protein expression.