發(fā)布時間：2018-07-14 22:22

【摘要】：目的探討PI3K-mTOR信號通路對蛛網(wǎng)膜下腔出血(subarachnoid hemorrhage,SAH)大鼠海馬區(qū)神經(jīng)細胞自噬的調控作用。方法成年雄性Sprague-Dawley大鼠隨機分為假手術組(n=24)、蛛網(wǎng)膜下腔出血模型組(SAH組,n=24)和LY294002組(n=24)。采用二次注血法制作SAH模型,假手術組不注血,LY294002組于造模前30min應用PI3K特異性抑制劑LY294002側腦室注射,對SAH大鼠進行預處理,注射劑量為500μmol/只。分別在出血后6、24、72、144hHE染色觀察海馬CA1區(qū)神經(jīng)細胞形態(tài)結構變化;免疫組化對PI3K、mTOR及Beclin-1和LC3-Ⅱ蛋白表達水平進行檢測。結果 SAH大鼠海馬CA1區(qū)神經(jīng)元數(shù)量明顯少于對照組(P0.05),PI3K-mTOR信號通路明顯被激活,自噬相關因子Beclin-1和LC3-Ⅱ的表達高于對照組(P0.05);LY294002組各時間點海馬CA1區(qū)神經(jīng)元數(shù)量明顯較SAH組減少(P0.05),PI3K-mTOR信號通路被抑制,相應自噬相關因子Beclin-1和LC3-Ⅱ的表達降低(P0.05)。結論 PI3K-mTOR信號通路通過激活神經(jīng)細胞自噬參與SAH后的細胞保護。
[Abstract]:Objective to investigate the regulation of PI3K-mTOR signal pathway on neuronal autophagy in hippocampal region of subarachnoid hemorrhagic hemorrhage rats. Methods Adult male Sprague-Dawley rats were randomly divided into three groups: sham operation group (n = 24), SAH group (n = 24) and LY294002 group (n = 24). The model of SAH was made by second injection of blood. In the sham operation group, 30min was injected into the ventricle of rats with PI3K specific inhibitor LY294002 before the model was made. The injection dose of LY294002 was 500 渭 mol/. The morphological and structural changes of neurons in hippocampal CA1 region were observed by HE staining at 6h, 72144h after hemorrhage, and the expression of PI3KnmTOR, Beclin-1 and LC3- 鈪，

本文編號：2123144