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目的观察人脑出血后血肿周围皮质内神经元血红素氧合酶-1(HO-1)与凋亡调节蛋白 Bcl-2的表达规律。方法剖解39例脑出血后不同时间死亡患者的脑组织,自出血灶边缘向外1～3 cm 及出血灶对侧相应部位的脑皮质组织进行取材,出血灶对侧设为对照组。采用免疫组化技术观察不同时间点出血灶周围 HO-1与 Bel-2的表达和变化规律,实验结果应用 SPSS 11.5软件进行统计学分析。结果 (1)人脑出血2 h 后就有 HO-1的表达,2～10 h 血肿周围神经元 HO-1阳性细胞数开始增加[(5.1±2.0)个/高倍视野],17～30 h 达到高峰[(11.3±0.9)个/高倍视野],120～216 h 后逐渐减弱[(8.6±0.8)个/高倍视野],240～408 h 时仍有 HO-1阳性神经元[(6.4±0.6)个/高倍视野](F=42.80,P<0.001)。对照组没有 HO-1表达。(2)Bcl-2阳性神经元在脑出血2～10 h 后就有表达[(4.2±1.7)个/高倍视野],17～30 h 血肿周围神经元 Bcl-2阳性细胞数开始增加[(6.6±0.5)个/高倍视野],36～96 h 达到高峰[(8.9±1.1)个/高倍视野],240～408 h 后逐渐减弱[(4.7±0.6)个/高倍视野](F=29.59,P<0.001)。对照组没有 Bcl-2阳性神经元的表达。(3)HO-1和 Bcl-2变化规律存在一定相关性(r=0.66,P<0.001)。结论人脑出血后出血灶周围皮质神经元内 HO-1与Bcl-2的表达增加,参与了脑出血后脑保护与脑损伤的作用机制。
Objective To observe the expression of heme oxygenase-1 (HO-1) and apoptosis-regulating protein Bcl-2 in the cortex around the hematoma after intracerebral hemorrhage in rats. Methods The brain tissue of 39 patients who died of cerebral hemorrhage at different time points was dissected. Cerebral cortex tissues of the corresponding parts of the hemorrhage were collected from the edge of the hemorrhage by 1 ~ 3 cm and contralateral to the hemorrhage as the control group. The expression of HO-1 and Bel-2 around the hemorrhagic lesions at different time points were observed by immunohistochemistry. The experimental results were analyzed by SPSS11.5 software. Results (1) The expression of HO-1 was detected 2 h after ICH, and the number of HO-1 positive cells began to increase (5.1 ± 2.0) / high power in 2 ~ 10 h after intracerebral hematoma, 17 ~ 30 h (11.3 ± 0.9) / high power fields], and gradually weakened [(8.6 ± 0.8) / high power fields after 120 ~ 216 h]. HO-1 positive neurons still remained after 240 ~ 0.6) pcs / high power field] (F = 42.80, P <0.001). The control group did not express HO-1. (2) The number of Bcl-2-positive neurons in Bcl-2 positive neurons increased from 2 to 10 hours after intracerebral hemorrhage [(4.2 ± 1.7) / high power fields] 6.6 ± 0.5) / high power field], peaked at 36-96 h [(8.9 ± 1.1) / high power fields], and gradually weakened [(4.7 ± 0.6) / high power fields after 240-480 h] , P <0.001). The control group did not express Bcl-2 positive neurons. (3) There was a certain correlation between HO-1 and Bcl-2 (r = 0.66, P <0.001). Conclusion The expression of HO-1 and Bcl-2 in cortical neurons around hemorrhagic focus after intracerebral hemorrhage is increased, which is involved in the mechanism of cerebral protection and brain injury after intracerebral hemorrhage.