脑出血患者血肿周围神经元凋亡及相关调控基因的观察  

Neural apoptosis and apoptosis-related genes in intracerebral hemorrhage patients

作　　者：吴成翰[1] 丁喜艳[1] 王海燕[2] 叶小包[1] 黄绳跃[3] 黄爱民[2] 李会忠[1] 吴松鹰[1] 余吉[3] 严晓华[3] 

机构地区：[1]福建中医学院第二临床医学院神经科,福州350003 [2]福建医科大学基础医学院 [3]福建省立医院

出　　处：《中华医学杂志》2006年第43期3073-3076,共4页National Medical Journal of China

摘　　要：目的观察脑出血(ICH)迟发性神经元死亡现象,了解人脑出血后血肿周围神经元凋亡及相关调节机制。方法对29例高血压脑出血血肿周围脑组织病理标本和6例非正常死亡3h内获取的脑组织标本,采用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测神经细胞凋亡率及免疫组织化学法检测Bcl-2、Bax、P53、半胱氨酸蛋白水解酶(caspase)-3蛋白表达水平。结果脑出血组与对照组细胞凋亡率分别为:4·10±0·28与0·57±0·43,Bcl-2分别为2·68±0·52与1·54±0·56,Bax分别为3·49±0·18与0·96±0·27,P53分别为4·12±0·63与0·96±0·71,caspase-3分别为3·50±0·25与0·74±0·73,前者明显高于后者,差异有统计学意义(均P<0·01)。Bcl-2、P53蛋白表达与细胞凋亡率呈负相关;Bax、caspase-3蛋白表达及Bax/Bcl-2与细胞凋亡率呈正相关。结论细胞凋亡机制参与了脑出血继发性损伤,是迟发性神经元死亡的主要原因,部分基因参与了神经元凋亡的调控,Bax、caspase-3促进凋亡,Bcl-2、P53抑制凋亡。Objective To observe the neural apoptosis and expression of apoptosis-related genes in brain in order to elucidate the regulation mechanism in the perihematomal region of intracerebral hemorrhage （ICH） patients. Methods Specimens of perihematomal region in human brain were obtained from 29 patients undergoing surgical evacuation of an intracerebral hematoma. Specimens of brain tissue were collected from the corpses of 6 persons within 3 hours after the accidental death. Neural apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridine 5 triphosphate nick end labeling （TUNEL） method and immunohistochemistry was used to detect the expression of Bcl-2, Bax, P53, and caspase-3 genes. Results The apoptosis rates of the ICH group was 4. 10 ±0. 28, significantly higher than that of the control group （0. 57 ±0. 43, P 〈0. 01 ）. The expression rate of Bcl-2 the ICH group was 2.68 ± 0. 52, significantly higher than that of the control group （ 1.54 ± 0. 56, P 〈 0. 01 ）. The expression rte of Bax of the ICH group was 3.49 ±0. 18, significantly higher than that of the control group （0. 96 ±0. 27, P 〈0. 01 ）. The expression of P53 was 4. 12 ±0. 63, significantly higher than that of the control group （0. 96 ±0. 71, P 〈 0. 01 ）. The expression of caspase-3 of the ICH group was 3.50 ± 0. 25, significantly higher than that of the control group （0. 74 ± 0. 73, P 〈 0. 01 ）. The expression levels of Bcl-2 and P53 were negatively correlated with the apoptosis rate （ both P 〈 0. 01 ）, while the expression levels of Bax and caspase-3, and the Bax/Bcl-2 ratio were positively correlated with the apoptosis rate in perihematomal region of ICH patients （ all P 〈 0. 01 ）. Conclusion Apoptosis is involved in the delayed brain injury after ICH in human and is the main factor of delayed neural death. Some of the genes take part in the regulation of neural apoptosis： Bax and caspase-3 hasten the apoptosis while Bcl-2 and P53 restrain it.

关 键 词：脑出血 神经元 凋亡 基因 

分 类 号：R743.34[医药卫生—神经病学与精神病学]