高血压脑出血血肿周围脑组织中TNF-α、VEGF以及ET-1的表达及其意义

The expression and significance of TNF-α, VEGF and ET-1 in the border zone after hypertensive intracerebral hemorrhage

目的探讨肿瘤坏死因子α（TNF-α）、血管内皮生长因子（VEGF）以及内皮素1（ET—1）与高血压脑出血继发性脑损伤的关系。方法将52例高血压脑出血患者血肿周围脑组织设为试验组，且按患者发病至手术的时间分为5组：≤6h组（6例）、〉6～12h组（15例）、〉12～24h组（16例）、〉24—48h组（7例）以及〉48～72h组（8例）。采用实时定量PCR法和免疫组织化学方法分别检测试验组和10例正常脑组织（对照组）中TNF-α、VEGF以及ET-1的表达，分析3种因子与高血压脑出血血肿周围脑组织损伤的关系。结果≤6h组、〉6～12h组、〉12～24h组、〉24—48h组以及〉48～72h组的TNF-α、VEGF以及ET—1mRNA表达水平均明显高于对照组（均P〈0．05）；并且随着发病时间的增加，TNF-α、VEGF以及ET-1mRNA的表达水平均表现为先升高而后降低。免疫组化检测结果表明，试验组TNF-α、VEGF以及ET-1的表达均高于对照组（均P〈0．05）。结论TNF-α、VEGF以及ET-1可能参与并促进了高血压脑出血后继发性脑损伤。

Objective To investigate the relationship between tumor necrosis factor alpha （TNF-α）, vascular endothelial growth factor （VEGF） and endothelin-1 （ET-1） with brain injury secondary to hypertensive intracerebral hemorrhage （HICH）. Methods Fifty-two patients admitted to Department of Pathology, Chengde Central Hospital with HICH （experimental group） were divided into 5 groups based on the time interval between illness onset to operation： ≤6 h group （6 cases）, 〉6 -12 h group （15 cases）, 〉 12 -24hgroup （16 cases）, 〉 24 -48 h group （7 cases） and 〉 48 -72 h group （8 cases）. The expression of TNF-α, VEGF and ET-1 in the border zone （brain tissues surrounding the hematoma） in the 52 patients and 10 normal controls were detected by real-time quantitative PCR and immunohistochemistry in order to explore the relationship of the factor expression to HICH-induced brain injury. Results The expression levels of TNF-α, VEGF and ET-1 mRNA in the ≤ 6 h group , 〉 6 - 12 h group, 〉 12 - 24 h group, 〉 24 - 48 h group and 〉 48 -72 h group were significantly higher than those in controls （all P 〈 0.05）, and their expression was increased first and then decreased as the illness progresses. The mRNA levels of TNF-α, VEGF and ET-1 in the experimental group were also significantly different when compared between different time points （all P 〈 0. 05）. Conclusion TNF-α, VEGF and ET-1 might be involved in and facilitate HICH-induced brain injury.