| Objective: Diabetes mellitus afflicts the central nervous system (CNS) mainly in increasing several risk and damage of brain vascular diseases such as stroke and leading to a chronic encephalopathy characterized by cognitive dysfunction. But the relative mechanism is not so clearly clarified. However, recently, many studies showed that oxidative stress caused by hyperglycemia played an important role in diabetic complications. Lactate dehydrogenase (LDH)is a kind of cytoplasm enzyme. When neuron cell membrane has a high permeability, LDH will be leaked out to the outside of the cell. After LDH enter into the blood, the content of it in the brain will decrease and its activities will weaken. So the LDH activities in the brain will reflect the brain injury. Na+-K+-ATPase is the most important enzyme in the biologic membrane. It plays an important role in maintaining membrane permeability, ionzing ingredients within the membrane and its outside and normal cell metabolism. Na~+-K~+ exchange with Na~+-K~+-ATPase catalyzed will occupy about 50% energy consumed in the brain, which is critical in maintaining the normal structure and functions of the cell. The decrease of Na+-K+-ATPase activity will cause Na+ increasing in the brain cell and the over-load of Ca2+, which will activate many kinds of enzymes to participate in the radical production and aggravate brain injury. Hyperglycemia caused by diabetes will stimulate the polyol pathway to produce plenty of radicals, the latter will cross react with protein and DNA macromolecules. Hippocaumpus is the advanced adjusting centrum which is sensitive to the oxidative stress. The radicals will intrude the unsaturated fatty acid in the membrane to produce many kinds of oxidative end-product involving malondialdehyde (MDA) which will destroy the cell membrane, endoplasmic reticulum, lysosome and mitochondria et al. Then it will lead to a series of functional disorder. The main hazard of MDA is that it can cross react with DNA and protein. When the double helix was crossed at the same time, the double helix can't disjoin in the next cleavage and lead to the cell death. If the protein is crossed, the protein will form the amorphic depositor. So some enzyme activities will decrease because of the destroyed structure.Furthermore, MDA will react with phospholipid, which aggravates the membrane disorder caused by the radicals. The change of MDA contents, LDH and Na+-K+-ATPase activities and hippocampus neuron cell cycle and its apoptosis have been investigated in this study to explore the role of oxidative stress in encephalopathy, which will furnish experimental theoretic basis to clarify the onset and developing mechanisms of diabetic central nerve system complications. Methods: Thirty four Wistar rats were divided into two groups at random, with half male and half female rats and weighting about 180 ±20 g. Diabetic rats were made by single intraperitoneal injection of 50 mg/Kg strepzotocin (STZ).The fasting uria glucose was measured after the rats were injected with STZ for 48 hours. Those animals with fasting uria glucose higher than "+++"would be measured fasting blood glucose after the rats were injected with STZ for 72 hours. Those animals with blood glucose higher than 16.7 mmol/L were regarded as diabetic rats. The normal rats were injected with an equivalent volume of citrate buffer. During the experiment, the rats had a free access to the water and food. The body weight and the uriaglucose were detected every week and the blood glucose was measured every other week. At the end of the 8th week, the rats were decapitated and the hippocampus was taken out. The hippocampus was made into tissue lysis liquid. The MDA contents, LDH and Na+-K+-ATPase activities were measured according to the detection kit. At the same time, the hippocampus was grinded into single cell suspension, the change of cell cycle and apoptosis were measured with flow cytometry under the dye of propidium iodide (PI). Results: Diabetic rats showed obvious polyuria, polyphagia, polydipsia and weight loss. Their blood glucose was higher than the normal control (P<0.01). At the end of the 8th week, the body weights of diabetic rats were significantly lower than the normal control (P<0.01). MDA contents in the diabetic rats hippocampus were significantly higher than the normal control (P<0.01),while the activities of LDH and Na+-K+-ATPase were significantly lower than the normal control (P<0.01) with detection of the spetrophotometer. The diabetic rats hippocamous neuron showed obvious G0/G1 phase arrest,while the normal control didn't show the phenomena. At the same time, hippocampus neuron apoptosis percentage of the diabetic...
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