Objective To probe the mechanism of anticonvulsant by melatonin from the angle of neurotransmitter.Methods Rat status epilepticus(SE) model was induced by pilocarpine(PILO).?-aminobutyric acid(GABA) content and glutamin acid decarboxylase(GAD)67 mRNA expression was detected at 6,48,72 h,and 7 d in the hippocampus of post-SE rats.The effect of melatonin on these changes was observed.Results GABA content was significantly lower in the hippocampus than in control(P

0.05).The positive rates of CD1a and CD83 in IL-18+TNF-? group were higher than those in other 2 groups.The positive rate of HLA-DR in IL-18+TNF-? group was higher than that in IL-18 group.No difference between IL-18 group and TNF-? group in the potency of stimulating T cell proliferation was found,whereas the stimulating potency in IL-18+TNF-? group was higher than that in IL-18 group and TNF-? group.IL-12 in IL-18+TNF-? group at 48 h and 72 h was higher than that in IL-18 group and TNF-? group(P

DC group.IL-12 secretion in IL-18/fusion group was higher than that in the fusion group,and IL-12 in the pulsed DC group was higher than that in the DC group.The in vitro killing rates of the 4 groups were 79.73%,50.68%,35.81% and 4.05%,respectively.Tumor forming time in IL-18/fusion group([12.82?2.85]d) was longer than those in the pulsed DC group([8.52?1.97]d,P

[ABSTRACT]AIM:ToinvestigatetheeffectoforidoninontheinvasionandmigrationofhumanlungcancerNCI-H460 cells.METHODS:NCI-H460 cells were divided into high-dose (HD), middle-dose (MD) and low-dose (LD) oridonin groups (cultured with 40, 20 and 10μmol/L of oridonin, respectively, as experimental groups), and normal (N) group ( treated without oridonin as control ) .The cell growth was observed .The cell proliferation was detected by MTT as-say.Boyden chamber was used to determine the cell invasive capacity .The cell migration was also measured .The levels of MMP-2 and MMP-9 were assayed by Western blotting .RESULTS:The cell counts in the experimental groups were lower than that in N group .The cell proliferation was inhibited as the inhibitory rates were 48.94%, 36.17%and 19.15% for HD group, MD group and LD group, respectively.The numbers of the invasive cells were 26.67 ±5.16 for HD group, 36.17 ±5.08 for MD group, and 44.33 ±5.50 for LD group.The migration rates in the experimental groups were lower than that in N group .The expression of MMP-2 and MMP-9 decreased dependent on the oridonin dose as follows: HD group

Objective To investigate the effects of crude extracted proteins from lesions of condyloma acuminata on immunophenotypes of dendritic cells.Methods Plastic-adherent mononuclear cells(MNCs)were isolated from umbilical cord blood or peripheral blood and cultured in media containing cytokines(GM-CSF,IL-4and LPS).The morphology and phenotypes of these cells were analyzed by flow cytometry and microscopy in12day's culture.Cells on the fourth day were incubated with crude extracts from lesions of condyloma acuminata,foreskin proteins,and PBS,respectively,followed by phenotypic analysis after9-12days' culture.Results Expression of antigens CD1a,CD80,CD86,MHC-I,MHC-II,CD14,CD54was detected after12days' cul-ture.It was shown that MNCs could be induced to differentiate to mature dendritic cells in our culture system.After incubation with crude extracts from lesions of condyloma acuminata for another9-12days,expression of CD86and HLA-DR was increased on dendritic cells.Conclusions Compared to foreskin and PBS pulsed dendritic cells,expression of CD86and HLA-DR is upregulated on dentritic cells after pulsing with condyloma acuminata lesion proteins.The data suggest that crude extracts from lesions of condyloma acuminata might enhance antigen-pre-senting capacity of dendritic cells and strengthen activation of T lymphocytes.

Objective To investigate the effects of essential fatty acids(EFA)on the contents of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the brain tissues of rats. Methods A total of 30 neonatal rats, 1 month old, were randomly divided into normal, EFA deficiency and fish oil supplement groups and given different feeding stuff for 3 months respectively. The contents of EPA and DHA in brain tissues were determined by high performance liquid chromatography (HPLC). Results As compared with normal group, the contents of EPA and DHA in EFA deficient group were significantly decreased(P

AIM: To investigate the role of nuclear factor ?B (NF-?B) in the induction of IL-8 gene by TNF-? in colon cancer cells and the effect of antioxidant on the induction of IL-8. METHODS: ELISA was used to detect the concentrations of IL-8. IL-8 mRNA was analyzed by using RT-PCR. NF-?B in the cell nuclei was detected with electrophoretic mobility shift assay. RESULTS: (1) IL-8 production and IL-8 mRNA expression induced by TNF-? was blocked by pyrrolidine dithiocarbamate (PDTC). (2) TNF-? triggered the activation and translocation of NF-?B and PDTC inhibited the activation of NF-?B induced by TNF-?. CONCLUSION: The induction of IL-8 gene and protein by TNF-? is dependent on the activation of NF-?B. Antioxidants may inhibit the induction of IL-8 gene and protein through inhibiting NF-?B activation.

Objective To observe the regulative effect of high dose of glucocorticoid (GC) on protein synthesis and mRNA transcription of corticotropin-releasing hormone (CRH) in paraventricular hypothalamic nucleus (PVN) so to ascertain whether there exists difference upon effect of GC either at high dose or at normal dose. Methods A total of 60 Wistar rats were divided into five groups, ie, blank control group, 10 -6 mol/L dexamethasone (DEX) group, 10 -9 mol/L DEX group, 9 g/L saline group and group that was treated with 10 -4 mol/L RU486 first and then with 10 -6 mol/L DEX. The drugs were given through femoral vein. CRH protein expression was measured by means of immunohistochemistry and laser confocal scanning microscophy (LCSM); CRH mRNA transcription level was investigated by in situ hybridization. Results There appeared positive CRH mRNA granules in cytoplasm of PVN after administration with 10 -6 mol/L DEX for 20 minutes but could be seen positive fluorescent granules of CRH protein 30 minutes later, which was reversed at an in advance blockage of GR, as was free in 10 -9 mol/L DEX group, 9 g/L saline group and blank control group. Conclusions High dose of GC can up regulate CRH gene expression in PVN and differs much from the traditional effect of GC at normal dose, as may be due to that high dose of GC exerts effects depending on membrane glucocorticoid receptor but normal dose of GC dose via iGR.

Objective To explore the expression and the changes of ski with time in the injured spinal cord in rats. Methods Sixty adult female Sprague-Dawley rats were randomly divided into sham group (n=30) and injury group (n=30), each group were further divided into 1 week, 2 weeks, 4 weeks, 8 weeks and 12 weeks subgroups, with 6 rats in each subgroup. Spinal cord injury at T10 was established with modi-fied Allen's technique (10 g × 25 mm) in the injury group. The hindlimbs behavior of rats was rated with Basso-Beattie-Bresnahan (BBB) scores 1 day, 3 days, 1 week, 2 weeks, 4 weeks, 8 weeks and 12 weeks after spinal cord injury. Three rats in each subgroup were stained with HE staining to observe the pathological changes of the spinal cord and the formation of cavity. The other 3 rats were analyzed with im-munofluorescence staining of ski and semi quantitative analysis. Results The BBB scores of each time point were less in the injury group than in the sham group (P<0.05). Necrosis was the major pathological change in the injury groups 1 and 2 weeks after injury;cystic cavity completely formed 4 weeks after injury, with dense scar tissue around it;there was no significant change in the cavity and scar 8 and 12 weeks after injury, however, the adjacent spinal cord was obviously thinner. Ski expressed little in the normal spinal cord, and expressed more and more after injury, peaked at 8 weeks and decreased then. Ski was mainly observed in white matter in the sham group and 12 weeks injury subgroup, which was in gray matter 2, 4 and 8 weeks after injury. Ski was highly expressed around the cavity in injury center and formed high expression band. Conclusion Ski expresses after spinal cord injury in rats, that may be associated with the activation and prolif-eration of astrocytes and the formation of glial scar.

Objective To explore the expression and change of ski-interacting protein (SKIP) in rats after spinal cord injury. Methods A total of 60 adult female Sprague-Dawley rats were randomly divided into sham group (n=30) and spinal cord injury (SCI) group (n=30), each group was further divided into five time points including one day, three days, five days, seven days, and 14 days with six rats in each time points. The model was established at T10 with modified Allen's technique, and the sham group only bit the lamina of rats. The hindlimbs behavior was assessed with Basso-Beattie-Bresnahan (BBB) score at each time point. The pathological changes of spinal cord neurons were detected with Nissl staining. The expression of SKIP were observed with immunofluorescence staining. Results The BBB scores were signif-icantly lower in each time point in SCI group than in the sham group (t>48.267, P<0.001). Compared with the sham group, Nissl bodies in the cytoplasm of spinal cord neurons began to disintegrate, coalesce and irregularly distribute, the neurons began to degenerate and die on the fifth day, and the damage deteriorated on the 14th day. Immunofluorescence staining showed that SKIP expression was mainly expressed in the gray matter of the spinal cord and little expressed in the white matter. The expression of SKIP gradually increased after SCI, and reached a peak on the fifth day (t=-17.035, P<0.001) and decreased significantly on the 14th day (t=3.853, P<0.05). Conclusion SKIP may be a new signaling molecule, which play an important role in neuronal apoptosis after SCI.