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目的探讨脑出血后血肿周围组织基质金属蛋白酶-9(MMP-9)和细胞间黏附分子-1(ICAM-1)的表达与脑水肿的关系。方法①解剖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组织进行取材,出血灶对侧设为对照组。②采用HE 染色、免疫组织化学技术观察不同时间点出血灶周围 MMP-9与 ICAM-1在脑组织中的表达和变化规律,实验结果应用 SPSS 11.5软件进行统计学分析。结果①脑出血2 h 后出血灶周围血管内皮细胞即有 MMP-9的表达[(1.2±0.8)个/高倍视野],5～10 h 后血肿周围 MMP-9阳性微血管数明显增高[(4.1±0.8)个/高倍视野],45～48 h 达到高峰[(10.6±1.4)个/高倍视野],96～120 h 后逐渐减弱[(5.0±1.1)个/高倍视野],与对照组比较,差异均有统计学意义(P<0.05),360～408 h 接近零表达。对照组没有 MMP-9表达。②脑出血后2 h 出血灶周围血管和神经细胞即有 ICAM-1的表达[(2.1±0.3)个/高倍视野],17～24 h 血肿周围 ICAM-1阳性微血管数开始明显增加[(6.0±1.1)个/高倍视野],72 h 达到高峰[(11.1±0.9)个/高倍视野],168～312 h 后逐渐减弱[(4.1±0.6)个/高倍视野],仍高于对照组(P<0.05)。此外,对侧脑实质内可见少量阳性神经细胞及 ICAM-1阳性微血管。③MMP-9和 ICAM-1之间有明显的相关性。结论脑出血后出血灶周围 MMP-9及 ICAM-1的表达增加,对脑出血后脑水肿的形成可能有促进作用;MMP-9与 ICAM-1之间可能有协同作用。
Objective To investigate the relationship between the expression of matrix metalloproteinase-9 (MMP-9) and intercellular adhesion molecule-1 (ICAM-1) and brain edema in patients with intracerebral hemorrhage. Methods ① Brain tissue of 39 patients with cerebral hemorrhage died at different time was dissected. The brain tissue of 1 ~ 3 cm outward from the edge of hemorrhage and the contralateral side of hemorrhage were drawn. Contralateral hemorrhage was set as control group. ② The expression of MMP-9 and ICAM-1 in the brain tissue around the hemorrhagic lesions at different time points were observed by HE staining and immunohistochemistry. The experimental results were analyzed by SPSS 11.5 software. Results ① After 2 h of intracerebral hemorrhage, the expression of MMP-9 in the vascular endothelial cells around the hemorrhage was significantly higher than that in the control group [(1.2 ± 0.8) / high power fields]. After 5 to 10 h, the number of MMP- ± 0.8) / high power field], peaked at 45 ~ 48 h [(10.6 ± 1.4) / high power fields] and gradually weakened [(5.0 ± 1.1) / high power fields after 96-120 h) , The differences were statistically significant (P <0.05), 360 ~ 408 h close to zero expression. The control group did not express MMP-9. (2) The ICAM-1 expression in blood vessels and nerve cells around the hemorrhage 2 h after intracerebral hemorrhage [(2.1 ± 0.3) / high power fields], and the number of ICAM-1 positive microvessels around hematoma began to increase significantly (1.1 ± 0.6) / high magnification field after 168 ~ 312 h] was still higher than that of the control group (P <0.01) P <0.05). In addition, a small amount of positive neurons and ICAM-1 positive microvessels were seen in the parenchyma. ③MMP-9 and ICAM-1 significant correlation between. Conclusion The increased expression of MMP-9 and ICAM-1 around hemorrhagic focus after intracerebral hemorrhage may promote the formation of cerebral edema after intracerebral hemorrhage. There may be a synergistic effect between MMP-9 and ICAM-1.