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检测实验性肝损伤小鼠肝组织丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）含量及血浆血栓素Ａ２（ＴＸＡ２）和前列环素（ＰＧＩ２）代谢产物的浓度，以探讨氧自由基（ＯＦＲ）及ＴＸＡ２－ＰＧＩ２在小鼠实验性肝损伤中的作用。结果表明，与对照组比较，肝损伤小鼠肝组织ＭＤＡ明显升高，且与血浆ＴＸＢ２变化呈正相关（ｒ＝０．９０８３，Ｐ＜０．０１）。ＳＯＤ明显降低；血浆ＴＸＡ２明显升高，ＰＧＩ２明显下降。以上结果提示ＯＦＲ与ＴＸＡ２／ＰＧＩ２平衡失调相互作用，共同引起实验性肝损伤。而乙肝Ⅰ号方可逆转ＭＤＡ、ＳＯＤ、ＴＸＡ２及ＰＧＩ２的变化
Detection of malondialdehyde (MDA) and superoxide dismutase (SOD) levels in the liver of mice with experimental hepatic injury and concentrations of plasma TXA2 and prostacyclin (PGI2) metabolites to investigate oxygen free radicals The role of (OFR) and TXA2-PGI2 in experimental liver injury in mice. The results showed that compared with the control group, the MDA in the hepatic tissue of liver injury mice was significantly increased, and was positively correlated with plasma TXB2 (r=0.9083, P<0.01). SOD decreased significantly; plasma TXA2 increased significantly, and PGI2 decreased significantly. The above results suggest that OFR interacts with TXA2/PGI2 imbalance and causes experimental hepatic injury. However, hepatitis B I can reverse the changes of MDA, SOD, TXA2 and PGI2