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目的观察D-氨基半乳糖加脂多糖诱导的急性肝衰竭大鼠脑组织中水通道蛋白-4(aquaporin-4,AQP4)表达情况,探讨其在急性肝衰竭(acute liver failure,ALF)继发性脑水肿中的作用。方法应用D-氨基半乳糖加脂多糖建立大鼠急性肝衰竭模型,腹主动脉采血检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、血氨(NH3)水平,RT-PCR和免疫组织化学技术分别检测脑组织内AQP4mRNA和蛋白的表达情况。结果与正常对照组比较,ALF组大鼠血清ALT、AST、NH3水平明显升高(P<0.01),AQP4mRNA和AQP4蛋白也显著升高[(1.15±0.25 vs 0.53±0.24)和(1.62±0.12 vs 1.41±0.11),均P<0.01]。结论急性肝衰竭时AQP4表达上调,AQP4在急性肝衰竭时脑水肿的形成过程中起重要作用。
Objective To investigate the expression of aquaporin-4 (AQP4) in the brain of acute hepatic failure induced by D-galactosamine and lipopolysaccharide (LPS) in rats, and to explore its role in the pathogenesis of acute liver failure (ALF) Role of brain edema. Methods Acute hepatic failure model was established by D-galactosamine plus lipopolysaccharide (LPS). Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood ammonia (NH3) Chemical techniques were detected AQP4 mRNA and protein expression in brain tissue. Results Compared with the normal control group, the levels of ALT, AST and NH3 in ALF group were significantly increased (P <0.01), and the levels of AQP4 mRNA and AQP4 protein were significantly increased in ALF group [(1.15 ± 0.25 vs 0.53 ± 0.24) and (1.62 ± 0.12 vs 1.41 ± 0.11), all P <0.01]. Conclusions AQP4 expression is up-regulated in acute liver failure and AQP4 plays an important role in the formation of cerebral edema in acute liver failure.