【摘要】：目的探討細胞自噬在孤獨癥發(fā)病中的作用。方法健康繁殖期Wistar雌鼠20只(250~260g),雄鼠10只(280~290g),按2∶1比例合籠過夜,次日早上陰道涂片發(fā)現(xiàn)精子計為孕1d。在其孕12.5d時,10只雌鼠腹腔注射丙戊酸鈉,其子代為孤獨癥模型組;10只注射同等劑量生理鹽水,其子代為正常組。通過比較自梳理實驗、三箱實驗驗證孤獨癥模型是否成功;Western blotting方法對比正常組與孤獨癥模型組大鼠生后42d(P42)海馬自噬相關(guān)蛋白LC3-Ⅱ、Beclin 1和P62表達的變化。結(jié)果 1.成功建立孤獨癥動物模型,與正常組比較,自梳理實驗顯示,模型組理毛時間較正常顯著增加(P0.05),三箱實驗結(jié)果顯示,模型組大鼠交互能力障礙、缺乏對新鮮事物的偏好性;2.與正常組相比較,模型組大鼠P42d海馬自噬相關(guān)蛋白LC3-Ⅱ表達顯著降低(P0.05),Beclin 1表達顯著降低(P0.05),P62表達顯著升高(P0.05)。結(jié)論孤獨癥大鼠P42d海馬自噬活性降低,提示增強自噬可能是一個潛在的治療策略。
[Abstract]:Objective to investigate the role of autophagy in the pathogenesis of autism. Methods 20 Wistar female rats (250 ~ 260g) and 10 males (280-290g) were used to spend the night in a cage in proportion to 2:1. The next morning vaginal smear showed that the sperm was pregnant for 1 day. On the 12th day of pregnancy, 10 female rats were injected intraperitoneally with sodium valproate, 10 rats in the autism model group were injected with the same dose of normal saline, and their children were the normal group. By comparing self-combing experiment and three-box experiment, we verified whether the autistic model was successful or not and whether the expression of LC3- 鈪，

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