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目的:观察肝性脑病模型组大鼠海马齿状回内神经元的变化及一氧化氮合酶(NOS)的表达,探讨海马神经元的形态学改变及一氧化氮(NO)在肝硬化和肝性脑病发病机制中的作用。方法:先对50只雄性大鼠进行Morris水迷宫测试,之后将动物分为正常对照组和实验模型组。9周后建立CCL4肝性脑病模型,分别取两组大鼠肝、海马组织进行HE染色、Nissl染色及NADPH-d染色。结果:(1)肉眼下可见模型组肝脏普遍呈坏死性肝硬化;(2)HE模型组血氨浓度明显高于正常对照组(P<0.05);(3)Nissl染色结果显示实验组大鼠海马神经元数目减少、染色较浅,胞浆内Nissl体减少或消失;(4)NADPH-d染色结果显示实验组可见粗大轴突着色,树突联系广泛;对照组则少有粗大轴突着色,树突间联系不如实验组广泛。实验组一氧化氮合酶(NOS)阳性神经元染色较对照组深,为紫蓝或深蓝色,且阳性神经元的数目较多。结论:(1)血氨增高是肝性脑病发病机制之一;(2)肝性脑病时海马受到损伤,并且一氧化氮(NO)可能介导了神经元的损伤。
Objective: To observe the changes of hippocampal dentate gyrus neurons and expression of nitric oxide synthase (NOS) in rat model of hepatic encephalopathy, and to explore the morphological changes of hippocampal neurons and the effects of nitric oxide (NO) on cirrhosis and The role of hepatic encephalopathy in the pathogenesis. Methods: Fifty male rats were subjected to Morris water maze test. Animals were then divided into normal control group and experimental model group. After 9 weeks, models of CCL4 hepatic encephalopathy were established. HE and Nissl staining and NADPH-d staining of the liver and hippocampus of the two groups were taken respectively. (2) The concentration of ammonia in HE model group was significantly higher than that in normal control group (P <0.05); (3) Nissl staining results showed that the rats in experimental group The number of neurons in the hippocampus decreased, the staining was lighter, and the Nissl body in the cytoplasm decreased or disappeared. (4) The results of NADPH-d staining showed that the axons in the experimental group were extensively stained and dendrites were extensively linked. , The contact between dendrites is not as good as the experimental group. Nitric oxide synthase (NOS) positive neurons in experimental group were deeper than the control group, purple or dark blue, and there were more positive neurons. Conclusions: (1) The increase of serum ammonia is one of the pathogenesis of hepatic encephalopathy. (2) The hippocampus is damaged in hepatic encephalopathy, and nitric oxide (NO) may mediate neuronal damage.