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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 phenomenon of delayed neuronal death in intracerebral hemorrhage (ICH), and to understand the apoptosis of neurons around the hematoma and the related regulatory mechanism after intracerebral hemorrhage. Methods Twenty-nine patients with hypertensive intracerebral hematoma around the hematoma and 6 cases of non-normal brain tissue samples were collected. The neuronal cells were detected by TUNEL The apoptosis rates and immunohistochemistry were used to detect the expression of Bcl-2, Bax, P53 and caspase-3. Results The apoptosis rates of ICH group and control group were 4.10 ± 0.28 and 0.57 ± 0.43, respectively. The Bcl-2 levels were 2.68 ± 0.52 and 1.54 ± 0.56 respectively , Bax were 3.49 ± 0.18 and 0.96 ± 0.27, P53 was 4.12 ± 0.63 and 0.96 ± 0.71, respectively, and caspase-3 was 3.50 ± 0. respectively 25 and 0 · 74 ± 0 · 73, the former was significantly higher than the latter, the difference was statistically significant (P <0.01). Bcl-2, P53 protein expression and apoptosis rate was negatively correlated; Bax, caspase-3 protein expression and Bax / Bcl-2 and apoptosis rate was positively correlated. Conclusion The mechanism of apoptosis is involved in the secondary injury of cerebral hemorrhage and is the main reason of delayed neuronal death. Some genes are involved in the regulation of neuronal apoptosis, Bax, caspase-3 promote apoptosis, Bcl-2, P53 Inhibit apoptosis.