摘要
目的:探讨急性肝坏死动物血脑屏障通透性异常改变. 方法:将280只♂Balb/c小鼠分为4组,应用内毒素(LPS, 10μg/kg)和D-氨基半乳糖(GalN,800 mg/kg)联合ip, 建立急性肝坏死小鼠模型.并检测血清ALT,观察肝脏组织病理学变化,利用伊文思蓝研究小鼠血脑屏障通透性的改变情况. 结果:单独应用LPS或GalN仅使血清ALT轻度升高,动物无死亡.而联合应用后ALT则从6 h开始明显升高(41.89±14.57μkat/L),到12h达高峰(170.30±16.13μkat/L), 较其他各组均有显著性差异(P<0.01).动物从6 h开始死亡,9 h达高峰,总死亡率达66.6%.肝脏HE染色可见大块或亚大块出血性坏死,而其他组仅见单个或灶状肝细胞坏死,部分细胞脂肪变性.并且脑组织EB含量在各时间点均较其他组明显升高. 结论:在急性肝坏死动物中存在血脑屏障通透性异常增加的改变,可能是引起脑水肿发生的重要机制.
AIM: To study the permeability of the blood brain barrier (BBB) in a mouse model of acute liver necrosis. METHODS: Male Balb/c mice were divided into 4 groups. In one group, mice were intraperitoneal of lipopolysaccharide (LPS, 10 μg/kg) with D-galactosamine (GaIN, 800 mg/kg) to induce acute liver necrosis. Other groups were controls. Serum levels of alanine transaminase (ALT) were determined and the liver tissues were fixed for histopathological analysis. The permeability of BBB in mice was investigated with Evans blue (EB). RESULTS: The serum levels of ALT were increased mildly in mice, which were administration of LPS or GaIN alone. And no animals died. But the levels of ALT began to increase at 6 hours (41.89±14.57 μat/L), and reached a maximal level at 12 hours (170.30±16.13 μat/L) after injection with both LPS and GaIN. Mice began to die at 6 hours, and at 9 hours after injection, the rate of lethality reached an extremely high level of 66.6%. The liver became massive or submassive necrosis. The concentration of EB in brain was significantly increased in ALF models compared with other groups. CONCLUSION: The permeability of BBB is increased in acute liver necrosis model. It may be the mechanism of the brain edema.
出处
《世界华人消化杂志》
CAS
2004年第6期1346-1348,共3页
World Chinese Journal of Digestology
基金
卫生部临床重点项目
No.97100252~~
