NO及NOS在Ⅰ型鸭肝炎病毒致雏鸭肝损伤机制中的作用

Effect of duck hepatitis virus typeⅠinduced liver injury on the NOS and NO levels in ducklings liver tissue

人工感染4日龄雏鸭病毒性肝炎模型,探讨一氧化氮合酶(NOS)和NO在Ⅰ型鸭肝炎病毒感染后的肝脏中的动态变化及与肝损伤的关系。120羽4日龄雏鸭随机分为试验组和对照组,试验组腿部肌注Ⅰ型鸭肝炎病毒,对照组注射等量生理盐水。感染后动态观察肝脏的病变、测定肝组织内NOS活性和NO的浓度以及肝组织内诱导型一氧化氮合酶(iNOS)的分布规律。结果显示,病毒感染后,雏鸭肝功能和肝脏结构都受到不同程度的损害;NO对肝脏的损伤在感染后3d内持续增强,从4d开始逐渐减弱;iNOS主要存在于雏鸭的巨噬细胞中,其含量在感染早期上升,后期逐渐下降;肝组织内NOS活性及NO的浓度变化与免疫组化显示结果一致。结果表明,鸭肝炎病毒感染的雏鸭肝脏的损伤程度与NOS、NO浓度变化一致,提示NO在鸭肝炎病毒导致的雏鸭肝损伤中起重要作用。

The present study aimed to elucidate the role of NO and NOS in duck hepatitis virus typeⅠ（DHVⅠ）-induced liver injury in 4 day-old ducklings.120 ducklings were divided into test group（80） intramuscular injected with DHVⅠand control group（40） injected with saline solution in the leg.Liver injury,NO level,NOS activity and positive immunohistochemistry for iNOS protein localized were examined in duckling liver.The results showed that DHV induced liver function failure and structure damage.Liver NO levels in the test ducklings continuously enhanced within 3 days post injection,and than gradully falled.INOS positive signals mainly located in the macrophages of livers,and their changes according with total NOS activity.These data suggest that DHVⅠ could induce liver injury in part via NO released by activation of NOS.