一些保肝药物对原代培养大鼠肝细胞糖原合成功能的影响

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 CL₁₅₀₀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。

INFLUENCE OF SEVERAL CHINESE DRUGS ON THE GLYCOGEN SYNTHESIZING FUNCTION OF PRIMARY CULTURED ADULT RAT HEPATOCYTES

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 CCl4-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 100 micrograms/ml concentration increased glycogen content of normal hepatocytes by 88%. It protected cells against CCl4-injury:BDD 10 micrograms/ml remarkably decreased CCl4-induced reduction of glycogen and 100 micrograms/ml showed complete protection. (2) Tremella poly-saccharide slightly increased glycogen content in normal cells, but in a concentration of 100 micrograms/ml it decreased CCl4-induced reduction of glycogen significantly. (3) Low concentration of norcatharidin (10 micrograms/ml) increased glycogen content of normal cells, but at 100 micrograms/ml concentration this effect disappeared. Furthermore, it intensified the toxic effect of CCl4 on glycogen at 10-100 micrograms/ml. (4) CL1500 (100 micrograms/ml) increased glycogen content of normal cells, but it intensified CCl4-injury effect on glycogen at the same concentration.