Objective:To observe the protective effects and possible mechanisms of dexmedetomidine(DEX)on hippocampal tissues of chronic sleep deprived(CSD)rats.Methods:Healthy male rats were divided into Control group,CSD group,CSD+DEX group,DEX group,and CSD+DEX+ANA-12 group.The CSD model was established by the modified multi-platform method(MMPM),and the rats were deprived of sleep for 18 hours per day for 21 days.DEX was combined with tyrosine kinase receptor B antagonist(ANA-12)for intervention.Starting at 7 days post sleep deprivation for 14 days.At the end of modeling,brain-derived neurotrophic factor(BDNF)protein in hippocampal neu-rons was determined by immunohistochemical staining;pro-inflammatory cytokines in hippocampal tissue homogenates were assessed by enzyme-linked immunosorbent assay;tyrosine kinase receptor B(TrkB)signaling proteins and cyste-ine protein hydrolase 3(caspase-3)were detected by Western blot.Results:Compared with the Control group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD group were significantly increased(P<0.05),while the expression level of BDNF in the hippocampal CA1 region was markedly reduced(P<0.05);Compared with the CSD group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD+DEX group were significantly reduced(P<0.05),while the expression level of BDNF in the CA1 region of the hippocampus was markedly increased(P<0.05);Compared with the CSD+DEX group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD+DEX+ANA-12 group were signifi-cantly increased(P<0.05),while the expression level of BDNF in the CA1 region of the hippocampus was markedly decreased(P<0.05).Conclusion:DEX inhibited CSD-induced hippocampal tissue damage.The possible mechanism is related to the regulation of BDNF/TrkB signaling by DEX.

Objective:To observe the protective effects and possible mechanisms of dexmedetomidine(DEX)on hippocampal tissues of chronic sleep deprived(CSD)rats.Methods:Healthy male rats were divided into Control group,CSD group,CSD+DEX group,DEX group,and CSD+DEX+ANA-12 group.The CSD model was established by the modified multi-platform method(MMPM),and the rats were deprived of sleep for 18 hours per day for 21 days.DEX was combined with tyrosine kinase receptor B antagonist(ANA-12)for intervention.Starting at 7 days post sleep deprivation for 14 days.At the end of modeling,brain-derived neurotrophic factor(BDNF)protein in hippocampal neu-rons was determined by immunohistochemical staining;pro-inflammatory cytokines in hippocampal tissue homogenates were assessed by enzyme-linked immunosorbent assay;tyrosine kinase receptor B(TrkB)signaling proteins and cyste-ine protein hydrolase 3(caspase-3)were detected by Western blot.Results:Compared with the Control group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD group were significantly increased(P<0.05),while the expression level of BDNF in the hippocampal CA1 region was markedly reduced(P<0.05);Compared with the CSD group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD+DEX group were significantly reduced(P<0.05),while the expression level of BDNF in the CA1 region of the hippocampus was markedly increased(P<0.05);Compared with the CSD+DEX group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD+DEX+ANA-12 group were signifi-cantly increased(P<0.05),while the expression level of BDNF in the CA1 region of the hippocampus was markedly decreased(P<0.05).Conclusion:DEX inhibited CSD-induced hippocampal tissue damage.The possible mechanism is related to the regulation of BDNF/TrkB signaling by DEX.

Objective:To observe the protective effect and possible mechanism of stellate ganglion block(SGB)on spatial learning memory function impairment in rapid eye movement sleep deprived(RSD)rats.Methods:Thirty-two rats were randomly assigned to Control group,RSD group,SGB group,and rapid eye movement sleep deprivation with stellate ganglion block intervention(RSD+SGB)group.The rats in RSD group and RSD+SGB group were modeled by modified multi-platform method(MMPM),and the rats in SGB group and RSD+SGB group were intervened by the SGB method.Morris water maze(MWM)was selected to evaluate the spatial learning and memory functions of rats in each group,and the expression levels of glutamate(Glu)and aspartate(Asp)in hippocampal tissues of rats in each group were detected by colorimetric assay,and the expression levels of N-methyl-D-aspartate receptor 1(NR1)and caspase-3 in hippocampal tissues of rats in each group were detected by Western Blot.Results:Compared with the RSD group,rats in RSD+SGB group had a significantly shorter escape latency after SGB intervention(P＜0.05),while the number of passes through the original platform position and the percentage of target quadrant time were significantly in-creased(P＜0.05);at the same time,the hippocampal tissues'expression levels of Glu,Asp,NR1,and caspase-3 were all significantly reduced(P＜0.05).Conclusion:SGB protects against RSD-induced impairment of spatial learn-ing memory capacity by reducing hippocampal tissue excitotoxicity and apoptosis induced by excitatory amino acid hyper-activation in RSD rats.

This study sought to clarify the molecular location and the interaction between mitoxantrone and mitoxantrone transforsomes. The anthraquinone of mitoxantrone, a heterocyclic ring that intercalates in the lipid of bilayer, was determined by UV-spectrophotometry and electron probes scan microscopy. Two aminoethylamino side-chains of the drugs fit to the phosphates of lecithin were determined by 8-value, thus the interaction with lecithin was substantiated. Differential scanning calorimetry confirmed that mitoxantrone has remarkable stabilizing effect on the mitoxantrone transforsomes membrane. The mitoxantrone binds tightly to lecithin. So a high degree of encapsulation efficiency and the sustained-release character of mitoxantrone transforsomes are verified.
Anthraquinones ; chemistry ; Calorimetry, Differential Scanning ; Delayed-Action Preparations ; chemistry ; Lecithins ; chemistry ; Mitoxantrone ; chemistry ; Spectrophotometry