Characterization of neuronal cell death in normal and diabetic rats following exprimental focal cerebral ischemia
Autor: | Yi-Bing Ouyang, Ying-Di Wang, Guang-Ren Li, Tong-Shu Yang, Gui-Xia Wang |
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Rok vydání: | 2001 |
Předmět: |
Male
Pathology medicine.medical_specialty Programmed cell death Ischemia Apoptosis Brain damage General Biochemistry Genetics and Molecular Biology Streptozocin Diabetes Mellitus Experimental Diabetes mellitus medicine In Situ Nick-End Labeling Animals Middle cerebral artery occlusion General Pharmacology Toxicology and Pharmaceutics Rats Wistar Cell Nucleus Electrophoresis Agar Gel Neurons Cerebral injury TUNEL assay business.industry Infarction Middle Cerebral Artery General Medicine DNA medicine.disease Flow Cytometry Rats Disease Models Animal Anesthesia Reperfusion Injury Hypoxia-Ischemia Brain medicine.symptom business |
Zdroj: | Life sciences. 69(23) |
ISSN: | 0024-3205 |
Popis: | We have studied the forms of cell death following ischemia/reperfusion, and the influence of diabetes mellitus (DM) as an additional factor. Based on the models of diabetes and middle cerebral artery occlusion (MCAO), characteristics of cell death after ischemia/reperfusion were evaluated synthetically by different methods: pathology, FCM, TUNEL and DNA agarose electrophoresis. The results showed that the occurrence of cerebral injury after ischemia/reperfusion was accompanied by cell necrosis and cell apoptosis. Cell apoptosis was mainly located in the ischemic penumbral (IP) zone around the densely ischemic focus. The ischemic core was characterized by cell necrosis. At the same time, the results showed that the process of ischemic cerebral injury worsened by DM was related to inducing cell apoptosis in IP and mid zone. In conclusion, there existed not only cell apoptosis but cell necrosis in brain damage following focal cerebral ischemia/reperfusion and showed a close, internal relationship between them. Brain damage following cerebral ischemia/reperfusion was worsened distinctly under diabetic conditions. |
Databáze: | OpenAIRE |
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