RESUMEN
[Objective] To investigate the effect of mitogen-activated protein kinases (MAPK) on cerebral ischemia induced by photothrombosis in Swedish amyloid precursor protein (APP/SWE) transgenic mice.[Methods] In APP/SWE transgenic mice and non-transgenic mice (n ＝ 12,respectively),photothrombotic stroke was induced,on 7 d after cerebral ischemia,the amount of the survival neuron in the penumbra was counted using Nissl staining (n ＝ 6),and the activities of p38MAPK and JNK were measured by Western blot (n ＝ 6).[Results] On 7 d after cerebral ischemia,ratio of amount of survival neuron over the penumbra in hippocampus in the ischemic side to that in the non-ischemic side in the non-transgenic mice group (78.3 ± 1.3)% was significantly higher than that in the APP/SWE transgenic mice group (70.5 ± 1.4)% (P ＜ 0.05);compared with the non-ischemic hemisphere,the activities of p38 MAPK and JNK increased significantly in the ischemic hemisphere in the APP/SWE transgenic mice group (P ＜ 0.05),whereas,there was no significant difference between ischemic and non-ischemic hemisphere in the non-transgenic mice group (P ＞ 0.05).[Conclusion] Photothrombosis causes more severe damage in the APP/SWE transgenic mice group than that in the non-transgenic mice group.The possible mechanism includes the increased activities of MAPK which enhance the process of neuronal cell apoptosis.
RESUMEN
BACKGROUND: Endothelial cell structural and functional integrity is importnat decisive fatcor for ischemic time-window and hemorragic transformation follwing brain ischemic injury.OBJECTIVE: To investiagte the endotheliocyt endurance to various course of ischemic injury basing on dynamical observation of morphological and ultrastructural changes of endotheliocyte during IR injury.DESIGN: Randomized controlled experiment.SETTING:Neurological Internal Department of the Second Affiliated Hospital of Jinan University.MATERIALS: This experiment was carried out in the Animal Experimental Laboratory of the Second Affiliated Hospital of Jinan University from March 1998 to March 1999. Totally 53 SD rats were randomly dihours of 6 rats.METHODS: Thread-bolt occlusion method was used to establish focal brain ischemia model on rats. Brain tissue was evenly cut into five coronary segments: namely A, B, C, D and E, segments C underwent TTC staining for marginal region location. segments D was taken for routine dehydration, transparency, envelop, slice and HE staining,optical microscopic observation. Ischemic surrounding area and central brain tissues was obtained from slice B, fixed and enveloped before cutting into ultrathin slices that was observed under transmission electron microscope.the occurring time of hemorrhagic infarction at different ischemic time cell vacuolization degree in foot process layer at different ischemic time points.RESULTS: Totally 53 rats were enrolled in this experiment and all data was entered into results analysis. Under optical microscope: Neuropil loose and small vascular surrounding edema was observed at ischemia 3 hours.Small arterial broken and hemorrhage occurred at ischemia 12 hours reperfusion 3 hours. Under electron microscope: Capillary endothelial nuclear swelling was observed at ischemia 3 hours, with cytoplasmic pinocytosi increasing and vacuolization in foot process layer appearing+; At ischemia 3 hours reperfusion 3 hours, the foot process layer vacuolization in center area was (++) and (+++) in marginal area; while at ischemia 6 hours reperfusion 3 hours, endothelia tight junction opened and vacuolization in foot process layer was (+++); pinocytosis was found obviously reduced after ischemia 12 hours reperfusion 3 hours, mitochondrial swelling was seldom observed, but tight junction increasingly opened and vacuolization in foot process layer appeared (+++) - (++++).CONCLUSION: Obvious structural changes of endotheliocyte appeared in post-ischemia 3 hours, endotheliocyte tight junction openning was observed at ischemia 6 hours, and hemorrage transformation occurred after ischemia 12 hours, mainly at the post-reperfusional ischemia center.