国际神经病学神经外科学杂志2012，Vol.39Issue(3)：229-234,6.
缺血后处理对大鼠脑缺血-再灌注中细胞凋亡的作用及其机制研究
Effects of ischemic postconditioning on apoptosis in cerebral ischemia-reperfusion injury in rats and its mechanisms
宫利 1王志 2邢诒刚 3李华1
作者信息
- 1. 烟台市毓璜顶医院神经内科,山东省烟台市264004
- 2. 中山大学附属第二医院麻醉科,广东省广州市510120
- 3. 中山大学附属第二医院神经内科,广东省广州市510120
- 折叠
摘要
Abstract
Objective To study the effects of ischemic postconditioning (IP) on apoptosis in cerebral ischemia-reperfusion (I/R) injury in rats, and possible mechanisms. Methods Focal cerebral ischemia rat model was developed by cauterizing the middle cerebral artery permanently and occluding the bilateral common carotid arteries temporarily. Rats were assigned randomly into following groups: Control, Sham-operated, I/R, IP, I/R + Z-DEVD-FMK and I/R + DMSO. Apoptosis, cytochrome c (cyt-c) and caspase-3 expression were detected by immunofluorescence staining and Western blot. Results The number of TUNEL-positive cells was lower in the IP group than in the I/R group (P<0.05). Some cells were cyt-c/TUNEL double-positive in the Sham-operated, IP, and I/R groups. But not all cyt-c positive cells were TUNEL positive. Cyt-c was released in a double hump-type in the I/R and IP groups ( 3 hrs and 48 hrs after reperfusion). The amount of released cyt-c in the IP group was much lower 48 hrs after reperfusion than in the I/R group (P < 0.05 ). The activity of caspase-3 increased 3 hrs after reperfusion, and peaked at 12 hrs and 24 hrs in the I/R group. The activity of caspase-3 in the IP group was lower than in the I/R group at each time point (P < 0. 05 ). The release of cyt-c in the I/R + Z-DEVD-FMK group was much less than in the I/R + DMSO group (P <0.01). The number of intact cell in ischemic penumbra in the I/R + Z-DEVD-FMK group was more than in the I/R + DMSO group (P < 0. 01). Conclusions IP can inhibit apoptosis of ischemic neurons after I/R. Cyt-c is involved in apoptosis of cerebral I/R injury in rats. There might be a feedback loop between cyt-c and caspase-3 in a focal cerebral ischemia rat model. IP plays a role in this loop.关键词
缺血后处理/脑缺血-再灌注/细胞凋亡/机制/大鼠Key words
ischemic postconditioning/ cerebral ischemia-reperfusion/ apoptosis/ mechanisms/rats引用本文复制引用
宫利,王志,邢诒刚,李华..缺血后处理对大鼠脑缺血-再灌注中细胞凋亡的作用及其机制研究[J].国际神经病学神经外科学杂志,2012,39(3):229-234,6.
