發(fā)布時間：2018-08-01 14:42

【摘要】： 目的:1.研究亞急性甲基苯丙胺中毒大鼠的一般行為學特點。2.研究Caspase-3和Bcl-2蛋白在甲基苯丙胺中毒損傷機制中所發(fā)揮的作用。 方法:40只健康雄性SD大鼠隨機分為對照組(n=10)和實驗組(又分為3個亞組,分別為末次注射后第1天、第4天、第7天組,n=10)。實驗組給予20mg/kg的甲基苯丙胺腹腔注射,對照組給予相同劑量的生理鹽水注射,每天注射兩次,注射時間為8:00,20:00,連續(xù)4天。每次注射后觀察動物的行為學改變。末次注射后分別于第1天、第4天、第7天分三批處殺。腹腔注射戊巴比妥鈉麻醉大鼠后用4%多聚甲醛灌注,取腦后置于4%的多聚甲醛中固定,石蠟包埋,作冠狀切片,行HE染色和免疫組化染色。用免疫組化技術對中毒大鼠相關腦區(qū)Caspase-3和Bcl-2的表達進行檢測,用圖像分析技術對檢測結果進行分析。 結果:Caspase-3和Bcl-2在大鼠腦的不同區(qū)域表達變化規(guī)律基本相似,均可見較明顯的陽性信號,Bcl-2在末次注射后第1天達到高峰,隨后表達下降,Caspase-3在末次注射后第4天達到高峰,隨后逐漸下降。Bcl-2峰值早于Caspase-3出現(xiàn)。 結論:1.亞急性甲基苯丙胺中毒動物模型成功建立。2.凋亡因子Caspase-3在甲基苯丙胺中毒大鼠相關腦區(qū)額葉皮質、紋狀體、海馬部位的異常表達,表明其參與了甲基苯丙胺神經毒性損傷。3.凋亡因子Bcl-2在甲基苯丙胺中毒大鼠相關腦區(qū)額葉皮質、紋狀體、海馬部位的異常表達,表明其與甲基苯丙胺神經毒性損傷保護機制密切相關。
[Abstract]:Purpose 1. To study the general behavioral characteristics of subacute methamphetamine poisoning rats. To study the role of Caspase-3 and Bcl-2 proteins in the mechanism of methamphetamine poisoning. Methods 40 healthy male Sprague-Dawley rats were randomly divided into control group (n = 10) and experimental group (n = 10). The experimental group was intraperitoneally injected with methamphetamine of 20mg/kg and the control group was injected with the same dose of normal saline twice a day for 8: 00 20: 00 for 4 days. Behavioral changes were observed after each injection. They were killed in three batches on day 1, day 4 and day 7 after the last injection. Rats anesthetized with pentobarbital sodium were injected intraperitoneally with 4% paraformaldehyde. The brain was fixed in 4% paraformaldehyde and embedded in paraffin. Coronal sections were made and HE staining and immunohistochemical staining were performed. The expression of Caspase-3 and Bcl-2 in the related brain regions of poisoned rats was detected by immunohistochemical technique and the results were analyzed by image analysis technique. Results the expression of Caspase-3 and Bcl-2 were similar in different regions of brain of rats. The positive signal of Bcl-2 reached its peak on the first day after the last injection, then the expression of Caspase-3 reached the peak on the 4th day after the last injection. The peak value of Bcl-2 was earlier than that of Caspase-3. Conclusion 1. The animal model of subacute methamphetamine poisoning was established successfully. The abnormal expression of apoptosis factor Caspase-3 in frontal cortex, striatum and hippocampus of rats with methamphetamine poisoning suggests that it is involved in the neurotoxicity injury of methamphetamine. The abnormal expression of apoptosis factor Bcl-2 in the frontal cortex, striatum and hippocampus of rats with methamphetamine poisoning suggests that it is closely related to the protective mechanism of methamphetamine neurotoxicity.
【學位授予單位】：昆明醫(yī)學院
【學位級別】：碩士
【學位授予年份】：2009
【分類號】：D919

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