硫化氢对短暂脑缺血/再灌注老年大鼠海马神经元Camkkβ、Bcl-2和Bax表达的影响  

Effect of hydrogen sulfide on Camkkβ、Bcl-2 and Bax in hippocampal neurons in transient global cerebral ischemia-reperfusion in aged rats

作　　者：刘志成 章以杰 宋晓丽 夏连春 常国江 刘涛 林俊 田苗苗 

机构地区：[1]浙江省宁波市红十字台胞医院神经内科,浙江宁波315731

出　　处：《中风与神经疾病杂志》2014年第8期704-706,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：目的探讨硫化氢对短暂脑缺血再灌注老年大鼠海马神经元Camkkβ、Bcl-2和Bax表达的影响。方法健康雄性SD老龄大鼠120只,随机分为对照组(C组)、缺血/再灌注组(IR组)、H2S组(H组)和生理盐水组(S组),采用Pusinelli四动脉阻断法建立全脑缺血模型。H组缺血前10 min腹腔内注射H2S外源性供体NaHS;S组注入等量生理盐水;C组不行任何处理。大鼠脑缺血/再灌注后24 h进行神经行为学评分;脑缺血/再灌注后1、3、5 d采用TUNEL法检测神经元的凋亡情况,采用Western-blot法测定大鼠海马内Camkkβ、Bcl-2和Bax蛋白表达。结果与对照组比较,缺血/再灌注组老年大鼠脑缺血/再灌注24 h后神经行为学评分升高,海马TUNEL阳性神经元计数升高,Camkkβ表达升高,Bcl-2表达下调,Bax表达上调(P<0.05);与缺血/再灌注组比较,H2S组老年大鼠脑缺血/再灌注24 h后神经行为学评分降低、海马区TUNEL阳性神经元计数降低、Camkkβ表达降低,Bcl-2表达上调、Bax表达下调(P<0.05)。结论硫化氢可通过降低神经元海马Camkkβ蛋白表达、上调Bc1-2蛋白表达、抑制Bax蛋白表达来减轻短暂脑缺血/再灌注损伤。Objective To study the effect of hydrogen sulfide on Camkkβ, Bcl-2and Bax in hippocampal neurons in transient global cerebral isehemia-repeffusion in aged rats. Methods One hundred twenty aged Spragne-Dawley rats were randomly divided into four groups for the experiment ： control group （ C group ） , ischemia/reperfusion group （ IR group） , H2S ＋ ischemia/repeffusion group （H group） and normal saline ＋ ischemia/repeffusion group （S group）. The global cerebral I/R was produced by 3 min four-vessel occlusion followed by repeffusion according to PulsineUi. NariS was gived by intraperitoneal injection 10 rain before establishing the model in H group. The same amount of saline was gived in S group. There was no processing in C group. The NBS was measured at 24 h of reperfusion. The apoptotic neurons and the expression of Camkkβ,Bcl-2 and Bax were detected by TUNEL and Western blot at 1,3 and 5 days of repeffusion. Result In the is- chemia/reperfusion group, the NBS, the number of apoptotic neurons and the amount of protein Camkkβ and Bax significantly increased, Bcl-2 reduced significantly （ P 〈 0. 05 ）. In comparison with the ischemia/reperfusion group, the NBS, the number of apoptotic neurons and the amount of protein Camkkβ and Bax significantly decreased, Bcl-2 significantly increased in the H group（ P 〈 0.05）. Conclusion Hydrogen sulfide can reduce transient global cerebral ischemia-reperfusion in rats. The possible mechanism is that it may decrease Camkkβ and Bax and increase Bcl-2 expression.

关 键 词：Camkkβ 硫化氢 老年人 再灌注损伤 

分 类 号：R743.31[医药卫生—神经病学与精神病学]