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Protective Effects of Peroxisome Proliferators Activated Receptors (PPARs) Agonist Rosiglitazone on Hippocampal Neuroton in Status Epilepticus Rats

Author: NiuHaiYan
Tutor: ZhengJiYing
School: Shanxi Medical
Course: Neurology
Keywords: Status epilepticus PPARγ agonists Bcl-2 Bax TUNEL Rosiglitazone
CLC: R742.1
Type: Master's thesis
Year: 2010
Downloads: 40
Quote: 0
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Objective: Peroxisome proliferator-activated receptors (peroxisome proliferators activated receptors, PPARs) is a ligand-activated transcription factor, is activated by its anti-inflammatory, anti-oxidation, anti-apoptotic mechanism is missing in the brain bloody disease, Parkinson's disease (PD), Alzheimer's disease (AD), a variety of nervous system disorders play a neuroprotective effect. The purpose of this experiment is to evaluate the role of rosiglitazone in rats status epilepticus. Continuous state by comparing the observed rat epilepsy in hippocampal Bcl-2, Bax protein expression and changes in TUNEL-positive cells, to investigate the status epilepticus rat protective effects and mechanism of rosiglitazone. Methods: 54 healthy adult male Wistar rats were randomly divided into model group, model drug group 24 (further divided into four sub-groups each time point, n = 6) and normal control group (6 only). Each group were selected gavage law will be dealt with. The control group and the model group were given normal saline; the Rosiglitazone solution the model drug group 4mg/kg/d given. Gavage 5d, in addition to the control group, the other groups were intraperitoneal injection of lithium chloride 127mg/kg, 18 h after intraperitoneal injection of fresh pilocarpine 30 mg / kg, and the control group were given saline by intraperitoneal injection. Status epilepticus in the the model drug group surviving rats orally, every 24 hours given rosiglitazone 4mg/kg model control group and normal control group to give normal saline. Model control group and model medication rats after SE 12 h for 24 h, 72 h, 7 d were sacrificed, the control group and were sacrificed 12 hours after SE group. All subjects hippocampus, TUNEL staining measured apoptosis and immunohistochemical measured Bcl-2, Bax, and calculate its Bcl-2/Bax ratio. Data using SPSS13.0 statistical analysis, P lt; 0.05 difference was statistically significant. Results: The model group hippocampus by TUNEL, Bcl-2, Bax cells compared with normal saline control group increased significantly (P lt; 0.05); rosiglitazone group of TUNEL-positive cells, Bax compared with the model group significantly reduce (P lt; 0.05 ), model group Rogge rosiglitazone group appear expression of TUNEL-positive cells at 12h, and gradually increased and peaked 48 hours, then gradually reduced until 7d, model group and rosiglitazone group Bax appear 12h expression and gradually increased and reached a peak at 24 hours, and then decreased gradually until 7d; rosiglitazone group Bc1-2 positive cells of Bcl-2/Bax ratio compared with the model group increased significantly (P lt; 0.05). Model group Bc1-2 after SE 12h obvious expression, followed by a gradual decline, 7d, close to the level of the control group, while the rosiglitazone group, Bcl-2 SE 12h after expression peaked at 24h, and then declined . Model group and the rosiglitazone group Bcl-2/Bax ratio peak at 12h, and then gradually decline. Conclusions: (1) rosiglitazone nerve cell damage in rat status epilepticus has a protective effect (2) the protective effect of rosiglitazone on the nerve cell damage in the rat status epilepticus with anti-apoptotic.

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CLC: > Medicine, health > Neurology and psychiatry > Neurology > Brain diseases > Epilepsy
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