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目的 观察乙醇诱导脂肪肝过程中肝组织一氧化氮合酶 (NOS)的表达 ,探讨不同亚型NOS表达与脂质过氧化的关系。方法 在大鼠饮水中加入乙醇建立乙醇性脂肪肝模型 ,采用免疫组化和逆转录多聚酶链反应 (RT PCR)的方法动态观察肝组织中NOS的蛋白及基因表达 ,同时检测肝组织中一氧化氮 (NO)、丙二醛 (MDA)含量。结果 成功建立乙醇性脂肪肝大鼠模型。与正常对照组相比 ,造模大鼠肝组织在第 4周时诱导型一氧化氮合酶 (iNOS)表达已显著增加 (P <0 .0 5 ) ,第 12周达高峰 ,而后有所下降 ,第 2 0周时又明显上升 (P <0 .0 1)。内皮型一氧化氮合酶 (eNOS)在第 4周时表达无明显改变 (P >0 .0 5 ) ,随造模时间延长而逐渐降低 (P <0 .0 5 )。肝组织中NO水平在第 4周时无明显升高 (P>0 .0 5 ) ,以后显著增加 ,第 12周达高峰 ,而后有所下降 ,第 2 0周时又明显上升 (P <0 .0 1)。肝组织中MDA含量在第 4周已显著升高 (P <0 .0 5 ) ,随饮用乙醇时间延长进行性增加。肝组织中NO、MDA含量与iNOS表达成正相关 (P <0 .0 1) ,与eNOS表达成负相关 (P <0 .0 1)。结论 乙醇诱导脂肪肝过程中肝组织NO水平升高主要与iNOS的活化有关 ,iNOS产生的NO可能与脂质过氧化损伤有关 ,而eNOS产生的NO可能起抗脂质过氧化损伤的保护作用。
Objective To observe the expression of nitric oxide synthase (NOS) in hepatic tissue induced by ethanol and explore the relationship between NOS expression and lipid peroxidation in different subtypes of fatty liver. Methods Ethanol was added into rat’s drinking water to establish a model of alcoholic fatty liver. The expression of NOS protein and gene in liver tissues was dynamically observed by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) Nitrogen (NO), malondialdehyde (MDA) content. Results The rat model of alcoholic fatty liver was successfully established. Compared with the normal control group, the expression of inducible nitric oxide synthase (iNOS) in the rat liver tissue at the 4th week was significantly increased (P <0.05), reached the peak at the 12th week, Decreased significantly at week 20 (P <0.01). The expression of endothelial nitric oxide synthase (eNOS) had no significant change at the 4th week (P> 0.05), and gradually decreased with the time of modeling (P <0.05). The level of NO in liver tissue did not increase significantly at the 4th week (P> 0.05), then increased significantly and reached the peak at 12th week, then decreased significantly (P <0 05) .0 1). The content of MDA in liver tissue increased significantly in the 4th week (P <0.05), and increased with the prolongation of drinking ethanol. The contents of NO and MDA in liver tissue were positively correlated with iNOS expression (P <0.01), and negatively correlated with eNOS expression (P <0.01). CONCLUSION: The increase of NO level in hepatic tissue induced by ethanol may be related to the activation of iNOS. NO produced by iNOS may be related to lipid peroxidation injury, while NO produced by eNOS may play an protective role against lipid peroxidation injury.