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目的分析血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)水平与脑出血大鼠继发性水肿程度及周围组织水通道蛋白-4(AQP4)表达的相关性。方法采用无肝素自体动脉血制作大鼠脑出血模型,分别于第1、2、3、5天检测大鼠血清TNF-α、IL-1β水平,同时分别于4个时间点各处死大鼠10只,采用干湿重法测定脑出血周围脑组织含水量,免疫组化ABC法染色检测AQP4阳性细胞表达率。观察不同时点血清TNF-α、IL-1β和脑组织含水量及脑组织AQP4阳性细胞表达率变化趋势。分析血清TNF-α、IL-1β水平与脑组织AQP4阳性细胞表达率的关系。结果造模第1、2、3、5天血清TNF-α、IL-1β、周围脑组织含水量及脑组织AQP4阳性细胞表达率均呈先升后降变化趋势,均于第3天达峰。血清TNF-α、IL-1β水平与脑组织AQP4阳性细胞表达率呈正相关(r=0.761;0.798,P<0.05)。结论脑出血后继发脑组织水肿程度与血清炎性反应因子水平、AQP4表达高低有关。出血后组织炎性反应及毛细血管通透性增加可能参与脑出血后继发脑水肿形成。
Objective To analyze the correlation between the level of serum tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and the degree of secondary edema in peripheral blood and the expression of aquaporin-4 . Methods The rat model of intracerebral hemorrhage was established by heparin-free autologous arterial blood. The level of serum TNF-α and IL-1β in rats were detected on the 1st, 2nd, 3rd and 5th day respectively. At the same time, rats were killed 10 Only the water content of brain tissue around cerebral hemorrhage was measured by dry-wet method, and the expression of AQP4 positive cells was detected by immunohistochemical ABC staining. The changes of serum TNF-α, IL-1β, brain water content and the expression of AQP4 positive cells in different time points were observed. The relationship between serum TNF-α and IL-1β levels and the expression of AQP4 positive cells in brain tissue was analyzed. Results At the 1st, 2nd, 3rd and 5th days after modeling, the contents of TNF-α, IL-1β in serum and the expression of AQP4 positive cells in brain tissue increased first and then decreased, all reaching the peak on the third day . Serum levels of TNF-α and IL-1β were positively correlated with the expression of AQP4 positive cells (r = 0.761; 0.798, P <0.05). Conclusions The degree of secondary brain edema after cerebral hemorrhage is related to the level of serum inflammatory response factor and the expression of AQP4. Post-hemorrhagic tissue inflammatory response and increased capillary permeability may be involved in the formation of secondary cerebral edema after intracerebral hemorrhage.