ABSTRACT
Objective To study any protection against hippocampal neuron damage induced by epilepsy (SE) provided by transcutaneous stimulation (TNS) of the trigeminal nerve and to document any effect of such stimulation on the expression of glutamic acid decarboxylase (GAD) 65/67.Methods Pilocarpine injection was used to induce epilepsy in healthy male Sprague-Dawley rats which were then randomly divided into a treatment group and a model group.Rats which had not received the pilocarpine injection served as normal controls.In the treatment group the rats were given electrostimulation for one month after the first spontaneous seizure following the injection of pilocarpine.In the model group they were given sham TNS for one month.After the month of stimula-tion,immunohistochemistry was used to detect the expression of GAD65/67 in the hippocampus.Terminal deoxy-nucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays and Nissl staining were applied to deter-mine apoptosis and neuron loss in the hippocampus.Results Significantly less apoptosis was observed in the treatment group than in model group at 24 h,48 h and 72 h post-injection.Compared to the model group,average GAD65/67 expression had increased significantly in the treatment group at 24 h,72 h,1 week,2 weeks and 4 weeks post-stimulation.GAD65 expression reached its peak from 72 h to 1 week post-stimulation,then decreased to the level of the control group by 4 weeks post-stimulation.The expression of GAD67 remained elevated at all the time points employed.Conclusions TNS can significantly protect hippocampal neurons from damage in epilepsy,at least in rats.The underlying anti-epileptic and neuroprotective mechanisms may involve increased inhibitory transmission induced by the stimulation.
ABSTRACT
The decoy receptor-3 ( DcR3 ) and glutamic acid decarboxylase-65 ( GAD65 ) recombinant adenovirus was construced and transduced into denlritic cells (DC). After the transduced DC were utilized to immunize NOD mice,the CD+8 T cells and blood glucose were analyzed. The results showed that recombinant adenovirus inhibited the proliferation and cytokine release of GAD65 specific T cells,and delayed the incidence of diabetes.Both interferon-γ[ (50.5±7.2)vs(95.4±6.9) and(91.2±6.5) pg/ml] and interleukin-2 [ (46.3±5.1 )vs ( 86.1 ±5.2 ) and ( 80.3 ± 7.3 ) pg/ml ] were decreased compared to those in negative and blank controls ( all P＜0.05 ).The results suggest that DcR3 and GAD65 recombinant adenovirus might provide a promising way for gene therapy of type 1 diabetes.
ABSTRACT
25 year).The patients were analyzed for the clinical characteristics.Autoantibodies to glutamic acid decarboxylase 65(GAD65-Ab),insulin(I-Ab)and autoantobodies to protein tyrosine phosphatase-like proteins(IA2-Ab)were assayed.HLA-DRB1,DQA1,DQB1 alleles(HLA-DRB1*03,*04,*09,*15,DQB1*0201,*0302,*0601,DQA1*0301,*0501)were typing by PCR-sequence specific primer(PCR-SSP).Results A little higher proportion of males,a longer duration of disease; a higher BMI and WHR characterized the adult-onset patients.The adults have a higher level of triglycerides and 120 min C-peptides than adolescent.The frequency and level of IA2-Ab of the adolescents were higher than adults(47.1% vs 15.1% and 0.46 U?mL~ -1 vs 0.07 U?mL~ -1 ,respectively,P