Effect of cardiotrophin-1 on neuronal loss of hippocampus and mossy fiber sprouting in status epilepticus rats
AIM: To investigate the effect of recombinant adenovirus cardiotrophin-1 (Adv-CT1) on the neuronal loss of hippocampus and the mossy fiber sprouting in status epilepticus (SE) rats and to determine whether CT-1 has protective effects on neuron damage after SE. METHODS: A lithium-pilocarpine induced SE model was used. SE-induced Wister rats were randomly divided into 2 groups (n = 6, each): CT-1 group (injecting Adv-CT1 in hippocampus) and model control group (injecting saline in hippocampus) , and another 6 rats served as normal control group (injecting saline intraperitoneally). At 14th day after SE, the morphological changes and neuronal loss in the CA1 subfield were examined by Nissl staining, mossy fiber sprouting (MRS) was examined by Timm staining, and the expression of caspase-3 in hippocampus was determined by integral optical density (IOD) immunohistochemical staining. RESULTS: Neuron degeneration and death in hippocampal formation were seen in model control group, but not in normal control group. The morphological changes in hippocampal formation in CT-1 group were milder than those in model control group. The number of neurons in the CA1 subfield in model control and CT-1 group was obviously lower than that in normal control group, while the number of neurons in CT-1 group was significant higher than that in model group (P < 0.05). Intensive MFS in the hippocampus was formed in model group. MFS stained band was also found in CT-1 group, but the score of MFS was significant lower than that of model group (P < 0.05). The expression of caspase-3 in hippocampal CA3 region was higher in model group than that in CT-1 group (P < 0.05). CONCLUSION: CT-1 has protective effects on neuron damage and checks SE-induced MFS by inhibiting the apoptosis of neurons through decreasing the expression of caspase-3.
status epilepticuscardiotrophin-1mossy fiber sprouting