【摘要】 目的用硫代乙酰胺（ＴＡＡ）诱发大鼠急性肝损伤，观察肝损伤过程中一氧化氮与自由基的变化．方法实验Ⅰ：大鼠２４只分为４组，一组为正常组，其余３组为损伤组．ＴＡＡ６００ｍｇ／ｋｇｓｃ２４，４８，７２ｈ测定内毒素及ＮＯ３－／ＮＯ２－，ＡＬＴ，ＡＳＴ含量．取肝组织匀浆，测定蛋白含量．脂质过氧化物歧化酶（ＳＯＤ）及谷胱甘肽过氧化物酶（ＧＳＨＰＸ）活性，并观察肝组织学变化．实验Ⅱ：大鼠３２只分为４组，Ａ组为正常组，Ｂ，Ｃ，Ｄ组ＴＡＡ６００ｍｇ／ｋｇｓｃ；同时给予Ｂ组生理盐水０４ｍＬ／ｋｇ，Ｃ组７５％ＬＡｒｇ３００ｍｇ／ｋｇ，Ｄ组２５％ＬＮＮＡ１０ｍｇ／ｋｇ．２４ｈ后重复注射１次．２４ｈ后按实验Ⅰ取血、肝组织，测定有关指标．结果大鼠注射ＬＡｒｇ后，ＮＯ的合成增多，转氨酶及肝组织损伤程度明显降低，注射ＬＮＮＡ组大鼠肝损伤程度加重，肝组织自由基的测定表明，抑制肝损伤大鼠ＮＯ合成，肝组织ＬＰＯ含量增高而ＳＯＤ，ＧＳＰＨＸ活性降低，ＳＯＤ，ＧＳＨＰＸ协同作用可清除体内自由基．结论抑制ＮＯ的生物合成，自由基水平增高，从而加重了肝损伤更多还原

【Abstract】 AIM To observe the formation and effects of nitric oxide (NO) and free radicals on acute liver injury induced by thioacetamide (TAA). METHODS ①Twenty four rats were randomly divided into four groups: One normal control group and three hepatic injury groups. The animals of injury groups were injected one single dose of TAA 600mg/kg sc. The blood content of endotoxin and NO 3 -/NO 2 -, ALT, ALT and AST at 24, 48 and 72 hours were measured. The protein content, activity of SOD and GSHPX were measured in liver homogenates. Meanwhile, the liver morpho pathology was examined. ②Twenty four rats were divided into four groups, A B,C and D.Group A was normal. Animals in groups B, C and D were given TAA 600mg/kg sc to induce acute liver injury. The rats of group B were given normal saline 0 4mL/kg ;group C, 7 5% L Arg (300mg/kg); group D, 2 5% L NNA (10mg/kg);and it was repeated 24 hours later. After another 24 hour, the blood and liver tissue were obtained and the relevant parameters assayed the same as in experiment one. RESULTS After L Arg was injected into rats, the synthesis of NO was increased, and blood transaminase and liver injury degree were significantly decreased. In group of rats injected with L NNA, the degree of injury was serious, indicating that NO had protective effect against hepatic injury induced by TAA. The free radicals in liver tissue inhibited the synthesis of NO in hepatic injury. The content of LPO in liver was increased, and the activities of SOD and GSHPX were lower. So the cooperation of SOD and GSHPX may eliminate the free radicals in vivo . CONCLUSION The inhibited biological synthesis of NO and increased level of free radical can aggravate liver injury.更多还原