RESUMEN
Objective To explore the role of caspase-3 activation and DNA fragmentation in later period of neonatal rat hypoxic-ischemic brain damage(HIBD). Methods DNA fragmentation,caspase-3 mRNA and caspase-3 protein were measured in 2 wks、3 wks and 4wks after setting HIBD animal model in newborn wistar rats by FCM, RT-PCR and Immunohistochemistry. Results (1) Apoptosis lasted 4ks after HIBD. This suggested a long lasting role of apoptosis in neonatal HIBD by TNNEL and EM.(2)Caspase-3 mRNA expression was estimated by semi-quantitative RT-PCR. It was higher in HIBD group(0.771?0.074) than in control group(0.620?0.038, P0.05. Average Avalue of Caspase-3 protein in HIBD group(0.374 ?0.038) at 3 wks was significantly higher than that in control group(0.356?0.020,P
RESUMEN
Epilepsy is a kind of brain dysfunction syndrome caused by so many reasons instead of a certain disease. Abnormal neuron discharge can cause epilepsy. Idiopathic epilepsy refers to epilepsy or epilepsy syndrome without any latent reasons but inherited trait. Idiopathic epilepsy is confirmed as an ion channelopathy at present. The first genemutation was found in idiopathic epilepsy in 1995, and a lot of genes coding either voltage-gated or ligand-gated ion channels have been found since then. In the present review, some new advances in research on ion channels dysfunction in idiopathic epilepsy are summarized.