摘要
目的探讨低氧预适应对小鼠急性脑梗死缺血半暗带神经元凋亡的影响,并对相关凋亡机制进行研究。方法将Blb/c近交系小鼠按照随机数字表法分为(1)正常对照组(N),无任何处理;(2)假手术组(C),仅行冷光源照射,不注射玫瑰红;(3)急性脑梗死组(CI),光化学法诱导小鼠脑皮质梗死模型;(4)低氧预适应+急性脑梗死组(HP+CI),低氧预适应后复制光化学法诱导小鼠脑皮质梗死模型。应用免疫荧光、激光共聚焦等技术检测模型制作成功后24h脑内缺血半暗带区细胞凋亡、Bcl-2、Bax和Caspase-3表达变化。结果 N组、C组小鼠大脑皮质偶见TUNEL阳性细胞,CI组和HP+CI组阳性细胞数明显增多,其中HP+CI组较CI组减少,差异有统计学意义(P<0.01)。CI组和HP+CI组的Bcl-2表达均分别非常显著地高于N组、C组,HP+CI组又显著地高于CI组。CI组和HP+CI组Bax的表达均分别非常显著地高于N组、C组,HP+CI组却非常显著地低于CI组。CI组和HP+CI组Caspase-3的表达均分别非常显著地高于N组、C组,但HP+CI组却非常显著地低于CI组。结论低氧预适应通过Bcl-2的高表达、Bax低表达和Caspase-3的低表达,抵御急性脑梗死缺血半暗带神经元凋亡,参与脑梗死保护机制。
Objective To explore the effects and mechanism of hypoxic preconditioning on the ischemic penumbra neuronal apoptosis in mice with acute cerebral infarction. Methods Blb/c mice were randomly divided into four groups： normal group（ N ） , sham operation group（C） , acute cerebral infarction group（CI） and hypoxic preconditioning and cerebral infarction group（ HP ＋ CI）. Immunofluorescence and laser confocal techniques were used to examine the fluorescence inten- sity change of Bcl-2 and Caspase-3 in the brain ischemic penumbra in 24h respectively after the model was successfully made. Results More TUNEL stained positive cells could be found on the cerebral cortex in group CI and HP ＋ CI. More TUNEL stained positive cells were found in group CI and HP ＋ CI than that in group N and C respectively. TUNEL stained positive cells decreased rapidly in group HP ＋ C｜ than that in group CI （P 〈0.01 ）. The expression of Bcl-2 in both group CI and HP ＋ CI were respectively and very significantly higher than that in group N and C ; and the expression in group HP ＋ CI was even higher than that in group CI. The expression of Bax in group CI and HP ＋ CI were also respectively and very significantly higher than that in group N and C ;whereas the expression in HP ＋ CI was significantly lower than that in CI. The expression of Caspase-3 in group CI and HP ＋ CI were also respectively and very significantly higher than that in group N and C ;whereas the expression in HP ＋ CI was significantly lower than that in CI. Conclusion Apoptosis of ischemic pe- numbra neuronal cells is depressed via increased expression of Bcl-2 and lowered activity of Bax and Caspase-3 in the ische- mie penumbra,acute cerebral infarction are thereby protected by hypoxic preconditioning.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2013年第9期792-796,共5页
Journal of Apoplexy and Nervous Diseases
基金
山东省自然科学基金(ZR2010HM029)资助
首都医科大学宣武医院基金(Z12111000190000)资助
