摘要
本文参照PO Seglen的方法并加以修改,建立了原代培养大鼠肝细胞糖原合成功能的测定体系。观察到联苯双酯既能使正常肝细胞合成糖原增加88%,又能保护肝细胞完全拮抗四氯化碳对其功能的损伤;银耳多糖能使四氯化碳对肝细胞糖原合成功能的损伤减轻57%;去甲斑蝥素10μg/ml能增加肝细胞糖原合成,浓度增加到100μg/ml时,此作用减弱,1000μg/ml则明显抑制糖原的合成,而且在10～100μg/ml浓度时,即能加强四氯化碳的损伤作用;100μg/ml CL_(1500)和熊果酸二钠单独应用可增加肝细胞糖原合成,但与四氯化碳同时应用,反而加重对糖原合成的抑制作用。
The influence of several Chinese drugs on the glycogen synthesizing function of normal and carbon tetrachloride-injured hepatocytes was investigated. Hepatocytes prepared from rats fasted for 16 h were incubated with 50 mmol/L glucose. Glycogen content was determined 30 and 90 min after incubation with normal and CCl_4-injured cells, respectively. Insulin was used as positive control which increased glycogen content and the data coincided with that in the literature. The following results were obtained (1) Biphenyl-dimethyl-dicarboxylate (BDD) in 100μg/ml concentration increased glycogen content of normal hepatoeytes by 88%.It protected cells against CCl_4-injury:BDD 10μg/ml remarkably decreased CCl_4-induced reduction of glycogen and 100μg/ml showed complete protection.(2)Tremella polysaccharide slightly increased glycogen content in normal cells,but in a concentration of 100 μg/ml it decreased CCl_4-induced reduction of glycogen significantly. (3) Low concentration of norcantharidin (10μg/ml) increased glycogen content of normal cells, but at 100μg/ml concentration this effect disappeared. Furthermore, it intensified the toxic effect of CCl_4 on glycogen at 10～100μg/ml. (4) CL_(1500) (100μg/ml) increased glycogen content of normal cells, but it intensified CCl_4-injury effect on glycogen at the same concentration.
出处
《药学学报》
CAS
CSCD
北大核心
1989年第9期653-658,共6页
Acta Pharmaceutica Sinica
基金
国家自然科学基金
关键词
保肝药物
肝细胞
糖原合成功能
Glycogen synthesis
Carbon tetrachloride
Biphenyl-dimethyldicarboxylate
Tremella polysaccharide
