Changes of expressions of tubulin and endosome-Iysosome system in neurons in hippocampus tissue of mice after status epilepticus and their significances / 吉林大学学报(医学版)

Objective: To investigate the changes of expressions of tubulin and endosome-lysosome in the neurons in hippocampus tissue of the mice after status epilepticus (SE), and to elucidate the change rule of microtubule and endosome-lysosome system in the process of delayed neuronal death. Methods: A total of 40 male ICR mice were divided into control group ( n= 7, given normal saline) and experiment group (w=33» give pilocarpine); the mice in experiment group met the SE standand were divided intoSE 1 d» SE 2 d, SE 3 d and SE 7 d groups according to the time after SE ( n=5). Nissl and Fluoro-Jade B (F-JB) staining methods were used to detect the damage of neurons in hippocampus tissue of the mice in various groups. The expression intensities of (3-tubulin? endosom protein Rab5 and lysosome constitutive protein LAMP1 and the percentages of (3-tubulin∗ Rab5 and LAMP1 positive areas in neurons in hippocampus tissue of the mice in various groups were detected by immunofluorescence method. The relationships between the expression of

Absence of Delayed Neuronal Death in ATP-Injected Brain: Possible Roles of Astrogliosis

Although secondary delayed neuronal death has been considered as a therapeutic target to minimize brain damage induced by several injuries, delayed neuronal death does not occur always. In this study, we investigated possible mechanisms that prevent delayed neuronal death in the ATP-injected substantia nigra (SN) and cortex, where delayed neuronal death does not occur. In both the SN and cortex, ATP rapidly induced death of the neurons and astrocytes in the injection core area within 3 h, and the astrocytes in the penumbra region became hypertropic and rapidly surrounded the damaged areas. It was observed that the neurons survived for up to 1-3 months in the area where the astrocytes became hypertropic. The damaged areas of astrocytes gradually reduced at 3 days, 7 days, and 1-3 months. Astrocyte proliferation was detectable at 3-7 days, and vimentin was expressed in astrocytes that surrounded and/or protruded into the damaged sites. The NeuN-positive cells also reappeared in the injury sites where astrocytes reappeared. Taken together, these results suggest that astroycte survival and/or gliosis in the injured brain may be critical for neuronal survival and may prevent delayed neuronal death in the injured brain.

Relationship between nitric oxide and superoxide dismutase in different brain tissues in delayed neuronal death rats / 吉林大学学报(医学版)

0. 05). When reperfusion time was prolonged, the level of NO in the experiment group was decreased gradually and was lower than that in control group (P

The investigation of apoptosis on the mechanism of cerebral vasospasm after subarachnoid hemorrhage / 医学研究生学报

Cerebral ischemia and reperfusion can cause delayed neuronal death in rodents,such as Mongolian gerbils and stroke-prone spontaneously hypertensive rats(SHRSP),which are used as an experimental stroke model.The protective effects of antioxidant nutrients such as vitamin E,green tea extract,ginkgo biloba extract,resveratrol,niacin and isoflavones in cerebral ischemia and reperfusion brain injury were reviewed.

Protective effects of dipfluzine against the whole cerebral ischemia and reperfusion injury in rats / 中国药理学通报

Aim To study the protective effects of dipfluzine against the whole cerebral ischemia and reperfusion injury and its mechanisms.Methods Four-vessel occlusion method was used to make the cerebral ischemia-reperfusion model.In early period of reperfusion,several including LDH,MDA,SOD and brain water content were tested.And in the late period of reperfusion,the delayed neuronal death and amnesia induced by reperfusion were studied.Results The contents of brain water and MDA were increased,and the activities of SOD and LDH were decreased after ischemia and reperfusion injury.The hippocampal structure and memory of rats were also destroyed in the delayed neuronal death.Dip reversed the changes obviously.It had antagonistic effect on brain edema and lipid oxidation,it also protected the neurons of hippocampal CA1 regions from ischemia injury.Conclusion Dip had protective effects on the early stage of reperfusion injury,and delayed neuronal death after the whole cerebral ischemia and reperfusion,which were possibly due to the antagonistic effect on lipid peroxidation.

Effects of glutamate receptor antagonists and protein synthesis inhibitor on delayed neuronal death induced by transient global ischemia in rat brain

It has been well documented that transient forebrain global ischemia causes selective neuronal degeneration in hippocampal CA1 pyramidal neurons with a delay of a few days. The mechanism of this delayed hippocampal CA1 pyramidal neuronal death (DND) is still controversial. To delineate the mechanisms of the DND, the effects of treatment with MK-801, an NMDA receptor antagonist, kynurenic acid, a NMDA/non-NMDA receptor antagonist, and/or cycloheximide, a protein synthesis inhibitor, on the DND were investigated in male Wistar rats. To examine the participation of apoptotic neuronal death in the DND, TUNEL staining was performed in ischemic brain section. Global ischemia was induced by 4-vessel occlusion for 20 min. All animals in this study showed the DND 3 and 7 days after the ischemic insult. The DND that occurred 3 days and 7 days after the ischemia were not affected by pretreatment with MK-801 (I mg/kg), but markedly attenuated by the pretreatment with kynurenic acid (500 mg/kg). Treatment with cycloheximide (1 mg/kg) also markedly inhibited the DND. The magnitudes of attenuation by the two drugs were similar. The magnitude of attenuation by co-treatments with kynurenic acid and cycloheximide was not greater than that with any single treatment. TUNEL staining was negative in the sections obtained 1 or 2 days after the ischemic insults, but it was positive at hippocampal CA1 pyramidal cells in sections collected 3 days after the ischemia. These results suggested that the DND should be mediated by the activation of non-NMDA receptor, not by the activation of NMDA receptor and that the activation of AMPA receptor should induce the apoptotic process in the DND.

Studies on the mechanism responsible for delayed neuronal death in hippocampus after transient cerebral ischemia in gerbils / 中国病理生理杂志

DND in the gerbil hippocampus was performed by bilateral occlusion of carotid arteries for 20 min followed by reperfusion 2 or 7 days. The contents of Ca~(2+) and MDA in drosal hippocampus were measured after two days reperfusion. Neuronal density in CA1 sector of hippocampus was used as an parameter. Effects of nimodipine and Superoxide dismutase (SOD) on DND in hippocampus were observed after 7 days reperfusion.The results indicated that the levels of Ca~(2+) and MDA were increased significantly. DND in hippocampal CA1 sector was ameliorated by both nimodipine and SOD significantly. It was suggested that Ca~(2+) and Iipid peroxidation play an important role in the development of DND hippocampus after transient forebrain ischemia in gerbils. Calcium Antagonist and free radical scavenger have obvious protective effects on DND in hippocampus.

A Morphological Study on Hippocampal Damage after Transient Cerebral Ischemia in Gerbils / 昆明医科大学学报

Gerbils were sacrificed at 12 hours,1,2,4 and 7 days after a 20 minute occlusion of both carotid arteries.The morphological changes of the dorsal hippocampus were observed at varying times of recirculation.Under a light microscope,the histopathologis changes of the hippocampus were observed in several subfields.The neurons in CA_1 sector were particularly sensitive to ischemia.The changes in the CAl subfield were very slow,and almost all of the pyramidal cells in the CAl sector were destroyed and disappeared after a 4 day recirculation. The CAl subfield was selected for electron microscopy,and an increase in the cisterns of the endoplasmic reticulum was observed after the 1-2 day recirculation.The results suggest that the hippocampal damage in CAl sector after transient cerbral ischemia is different from the neuronal damage of the other parts of the brain.Delayed neuronal death and selective vulnerability were the main characteristics.