絞股藍皂苷複方對四氯化碳和半乳糖氨誘發大白鼠急性肝中毒之治療效果

Therapeutic Effects of Gypenoside Formulas on Acute Hepatotoxicity Induced by CCL4 and D-Galactosamine in Rats

本研究目的擬探討絞股藍皂苷複方，對四氯化碳和半乳糖氨誘發大白鼠急性肝中毒的治療效果。實驗各分成六組，每組8隻，A組為正常對照組，B組為肝中毒，C至E為治療組，C組為絞股藍皂苷一號方（單味絞股籃總皂苷），D組為絞股藍皂苷二號方（絞股藍總皂苷加聯苯雙脂），E組為絞股藍皂苷三號方（絞股藍總皂苷加聯苯雙脂、丹參），F組為Silymarin藥物參考組。實驗結果，所有治療組及藥物參考組對四氯化碳和半乳糖氨肝中毒的血清SGOT、SGPT生化值上升變化，均有顯著降低作用。各藥物組間的比較，絞股藍皂苷二號方及三號方治療四氯化碳肝損傷，其降低血清酵素的指數，比絞股藍皂苷一號方療效佳，有明顯保肝作用；而治療半乳糖氨肝中毒，各藥物組間的比較，均無統計學上的差異。絞股藍皂苷複方和Silymarin治療四氯化碳肝中毒的病理組織觀察，依Jonker's病理半定量分析顯示，絞股藍皂苷一號方有減輕肝細胞發炎、減少肝細胞有絲分裂的作用，絞股藍皂苷二號方有減輕肝細胞發炎、肝脂肪病變、減少肝細胞有絲分裂及減少膽管增生等作用，絞股藍皂苷三號方有減輕肝細胞發炎、肝脂肪病變、肝細胞壞死等作用。其治療半乳糖氨肝中毒的病理組織觀察，依Jonker's病理半定量分析，絞股籃皂苷一號方對抗細胞壞死、抗膽管增生等，絞股藍皂苷二號方對玻璃樣變性、脂肪病變、抗細胞壞死、及抗膽管增生等，絞股藍皂苷三號方對玻璃樣變性、脂肪病變及抗膽管增生等均有顯著的療效，然而此三方及藥物參考組均無顯著抗肝細胞發炎的作用。

The purpose of study was to investigate the therapeutic effects of Gypenoside Formulas (GFs) on acute hepatotoxicityh induced by CCL?? and D-galactosamine (D-GalN) in rats. The experimental animals were divided into 6 gourps of each 8 rats. A group was a normal control and B group was CCL induced hepatotoxicity. Group C, D and E were treated with GF-1 (Gypenoside), GF-2 (Gypenoside + bifenbate), and GF-3 (Gypenoside + bifenbate + dan-shen) respectively. Group F was treated with reference drug (silymarin). The results demonstrated that the GFs and the reference drug were markedly decreased the biochemical elevated serum levels of SGOT and SGPT in the acute CCl?? and D-GalN induced hepatotoxicity. Further analysis of the drug-treated groups indicated that the effects of GF-2 and GF-3 were the most potent with an obvious hepatoprotection. However, it was not statistical significance among the drug treated groups for D-GalN induced hepatotoxicity. The GFs and silymarin treated the CCL?? hepatotoxicity, the pathological lesion showed a various improvement by Jonker's semiquantitative analysis. The GF-1 decreased liver cell inflammation and mitosis, the GF-2 improved the hepatocytes inflammationj, mitosis, fatty change and decreased the bile duct proliferation, the GF-3 improved inflammatory cells infiltration, cellular necrosis and fatty change had a statistically significant effects. The drug groups treated the D-GalN hepatotoxicity according to the Jonker's pathological semiquantitative analysis, the results revealed that the GFs had an obviously various effectiveness. The GF-1 was significantly hyaline degeneration, fatty change, cell necrosis and bile ducts proliferatin. And the GF-3 improved the hyaline degeneration, fatty change and bile ducts proliferation with statistical significance. In this study the GFs and silymarin were not statistical significance on anti-hepatocyte inflammation induced hy D-GalN hepatotoxicity.