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目的:探讨肝细胞生长因子(HGF)在脂多糖致幼年大鼠脑损伤中的变化及意义。方法:1月龄SD大鼠160只,随机分为2组。脂多糖组(n=80),颈外动脉注射脂多糖建立脑损伤模型;对照组(n=80)颈外动脉注射等量生理盐水。于注射后6、12、24、48及72h处死大鼠,置备脑组织标本。甲酰胺法测脑组织伊文思蓝(EB)含量,免疫组织化学法检测脑组织HGF、神经元特异性烯醇化酶(NSE)、胶质纤维酸性蛋白(GFAP)的表达,RT-PCR检测HGF mRNA的表达,同时观察脑组织病理变化。结果:脂多糖组脑组织EB含量、NSE、GFAP蛋白表达水平均于脂多糖注射6h后增加,24h达高峰(P<0.05);HGF蛋白及mRNA表达亦于脂多糖注射后6h增加,48h达高峰(P<0.05)。对照组上述指标无明显变化(P>0.05)。脂多糖组脑组织HGF蛋白表达水平与EB含量、NSE和GFAP蛋白含量成正相关(r分别为0.954、0.927、0.974,P<0.01);HGF蛋白与mRNA表达成正相关(r=0.974,P<0.01)。结论:HGF参与了感染性脑损伤的病理发展及修复过程。
Objective: To investigate the changes and clinical significance of hepatocyte growth factor (HGF) in brain injury induced by lipopolysaccharide in young rats. Methods: One-month-old SD rats 160 were randomly divided into two groups. Lipopolysaccharide group (n = 80), the model of traumatic brain injury was established by injecting lipopolysaccharide into the external carotid artery. The control group (n = 80) received the same amount of saline injected into the external carotid artery. Rats were sacrificed at 6, 12, 24, 48 and 72 h after injection, and the brain tissue samples were prepared. The contents of Evans blue (EB) in brain tissue were measured by formamide method. The expression of HGF, neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP) in brain tissue were detected by immunohistochemical method. mRNA expression, while observing pathological changes in brain tissue. Results: The levels of EB, NSE and GFAP in lipopolysaccharide group increased at 6h after injection of lipopolysaccharide and peaked at 24h (P <0.05). The expression of HGF protein and mRNA increased at 6h after lipopolysaccharide injection, reached the peak at 48h Peak (P <0.05). There was no significant change in the above indexes in the control group (P> 0.05). The expression of HGF protein in brain tissue of lipopolysaccharide group was positively correlated with EB content, NSE and GFAP protein content (r = 0.954,0.927,0.974, P <0.01). HGF protein was positively correlated with mRNA expression (r = 0.974, P <0.01) ). Conclusion: HGF participates in the pathological development and repair process of infectious brain injury.