论文部分内容阅读
采用D-氨基半乳糖(D-GaIN)诱导大鼠急性肝损害模型,实验分成正常组、模型组、肝炎平组及肝得健组。观察了血清中丙氨酸氨基转移酶(ALT)、TGF-α、肝细胞及红细胞中过氧化物(LPO)和肝组织及红细胞超氧化物歧化酶(SOD)的变化。结果表明:肝炎平和肝得健组血清中ALT、TGF-α及LPO与模型组相比明显下降(P<0.01),而肝炎平和肝得健组SOD活性分别是(594.7±164.8)、(575.0±174.5)U/g,明显高于模型组(417.64±139.5)U/g(P<0.01)。提示肝炎平能抗肝损害时肝组织氧自由基(FR)的产生,降低血浆和组织中LPO的水平,并能提高细胞SOD的活性,从而减轻肝损伤。其对肝细胞的保护作用与肝得健一致。
Acute hepatic injury in rats was induced by D-galactosamine (D-GaIN). The experimental groups were divided into normal group, model group, Hepatitis group and Gandejian group. The changes of serum alanine aminotransferase (ALT), TGF-α, hepatocyte and erythrocyte peroxide (LPO) and hepatic tissue and erythrocyte superoxide dismutase (SOD) were observed. The results showed that the levels of ALT, TGF-α and LPO in the serum of Hepatitis-Ping He He DeJian group were significantly lower than those in the model group (P<0.01), while the SOD activities in the Hepatitis-Ping He Gan De Jian group were (594.7±164.8) and (575.0) respectively. ±174.5)U/g, significantly higher than the model group (417.64±139.5) U/g (P<0.01). It is suggested that Hepatitis Ping-Peng can prevent the liver from damaging hepatic tissue when hepatic tissue produces oxygen free radicals (FR), reduces plasma and tissue LPO levels, and can increase the activity of SOD in cells, thus reducing liver injury. Its protective effect on liver cells is consistent with that of liver.