论文部分内容阅读
本文采用整体动物实验方法,通过生化、组织化学等观祭,研究了乙肝Ⅰ号抗四氯化碳肝损伤之原理结果表明:乙肝Ⅰ号按12.5％/ml/只/日预防性给予,可明显抑制给药组动物sGPT、sGOT的增高;对蛋白的合成亦有促进作用;并可使实验动物ATP酶、琥珀酸脱氢酶明显增高,且与联苯双酯对照组结果十分接近(p<0.05),说明乙肝Ⅰ号实验组对四氯化碳肝损伤有一定的保护作用。
This article adopts the whole animal experiment method, and through the observation of biochemistry, histochemistry etc., studies the principle of hepatitis B anti-CCl liver injury. The results show that: Hepatitis B No. I is preventively given by 12.5%/ml/only/day. The sGPT and sGOT were significantly inhibited in the animals in the administration group; the protein synthesis was also promoted; and the ATPase and succinate dehydrogenase in the experimental animals were significantly increased, and the results were similar to those in the bifendate control group (p <0.05), indicating that hepatitis B experimental group has a protective effect on carbon tetrachloride liver injury.