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目的探讨脂肪肝缺血再灌注损伤过程中丙二醛、谷丙转氨酶、内皮素、肿瘤坏死因子的变化,以及维拉帕米对脂肪肝缺血再灌注(I/R)损伤的保护作用。方法通过建立脂肪肝动物模型,观察脂肪肝大鼠在缺血前门静脉压力,缺血前、缺血15min 和30min 再灌注60min 后血清谷丙转氨酶(ALT),肿瘤坏死因子(TNFα),内皮素(ET-1)和肝组织中丙二醛(MDA)的变化,以及维拉帕米对 I/R 损伤的保护作用。结果缺血前及 I/R 损伤后,脂肪肝组大鼠肝组织中 MDA 及血清 ET-1、TNFα、ALT 呈升高趋势,药物组则明显降低。结论 (1)肝脂肪变性可导致肝窦狭窄和不规则,门静脉压升高。(2)含大量脂质的肝细胞对 I/R 损伤敏感性增高,通过产生过多的 MDA,ET-1,TNFα,导致肝细胞破坏,血清 ALT 升高。(3)缺血前应用维拉帕米,对脂肪肝 I/R 损伤起保护作用。
Objective To investigate the changes of malondialdehyde, alanine aminotransferase, endothelin and tumor necrosis factor during the process of hepatic ischemia-reperfusion injury and the protective effect of verapamil on the hepatic ischemia-reperfusion (I / R) injury in fatty liver. Methods The fatty liver model was established in rats with fatty liver to observe the changes of serum alanine aminotransferase (ALT), tumor necrosis factor (TNFα), endothelin (ET-1) and malondialdehyde (MDA) in liver tissue, and the protective effect of verapamil on I / R injury. Results Before ischemia and after I / R injury, the content of MDA and serum ET-1, TNFα and ALT in fatty liver group increased significantly, while the drug group decreased significantly. Conclusions (1) Hepatic steatosis can lead to stenosis and irregular hepatic sinusoids and elevated portal pressure. (2) The hepatocytes with a large amount of lipids had an increased sensitivity to I / R injury, which resulted in the destruction of hepatocytes and the increase of serum ALT by producing excessive amounts of MDA, ET-1 and TNFα. (3) application of verapamil before ischemia, protective effect on I / R injury of fatty liver.