一氧化氮在实验性肝损伤中的作用  

Effects of nitric oxide in experimental liver disease

作　　者：郑晓宾[1] 韩德五[1] 马学惠[1] 高飞[1] 许瑞龄[1] 赵元昌[1] 

机构地区：[1]山西医科大学病理生理教研室,太原030001

出　　处：《中国病理生理杂志》1999年第12期1090-1093,共4页Chinese Journal of Pathophysiology

基　　金：卫生部基金资助

摘　　要：目的：观察３ 种细胞因子对体外培养大鼠肝细胞产生一氧化氮（ ＮＯ） 的影响及ＮＯ 在实验性肝损伤中的作用。方法与结果：给大鼠注射内毒素后分离肝细胞，培养液中加入细胞因子（γ－ ＩＦＮ，ＩＬ－ ２ ，ＴＮＦ－ α） ，上清液中ＮＯ 含量增加，两种以上细胞因子联合应用，ＮＯ 含量增加更明显；大鼠注射内毒素及Ｌ－ 精氨酸，血清中ＮＯ 含量增加，肝损伤减轻；大鼠给硫代乙酰胺（ＴＡＡ） 灌胃，并注射ＮＯ 生成抑制剂Ｌ－ ＮＮＡ，动物出现嗜睡及肝昏迷脑电图，血浆ＬＤＨ、Ｃｒ升高。结论：内毒素及细胞因子促进ＮＯ 合成，ＮＯ 在内毒素诱发的肝损伤及ＴＡＡ 致肝功能不全中具有对抗作用。AIM: To investigate the role of cytokine to nitric oxide (NO) production and the effects of NO in hepatic injury in rats. METHODS and RESULTS: 1.Hepatocytse pretreated with lipopolysaccharide (LPS) responded to in vitro stimulation for 20 h by tumor necrosis factor-α(TNF-α),γ-interferon( γ-IFN) or interlukin-2 (IL-2) with enhanced NO formation. Two or three kinds of cytokines in combination, production of NO was higher than any single one. 2. Rats were injected with LPS+L-Arginine or LPS+L-NNA, NO levels were higher and alanine aminotransferase (ALT) contents were lower in rats of LPS+L-Arg group than in rats of LPS group(NO:162 78±18 34 μmol/L vs 95 5±50 74 μmol/L, P <0 01, ALT:54 36±9 23 U/L vs 118 73±44 9 U/L). NO decreased and ALT increased in rats of LPS+L-NNA group. 3. Rats were given thioacetamide (TAA) or TAA+L-NNA. The TAA+L-NNA group rats were sleepy and presented δ waves in electroencephalogram. Lactate dehydrogenase (LDH) and creatinine (Cr) contents in plasma were higher in rats of TAA+L-NNA group than TAA group(LDH:854±87 48 U/L vs 570 72±116 74 U/L, Cr:361 04±153 68 mg/L vs 153 4±28 9 mg/L). CONCLUSIONS: 1.The results indicated that modulation of NO generation by cytokines in vitro in hepatocytes. 2. NO plays a protective action against liver injury and hepatic dysfunction induced by LPS or TAA.

关 键 词：一氧化氮 细胞活素类 肝损伤 大鼠 

分 类 号：R575.02[医药卫生—消化系统]