刘耕陶, 魏怀玲, 宋振玉. 联苯双酯对小鼠肝损伤保护作用的进一步研究J. 药学学报, 1982, 17(2): 101-106.
引用本文: 刘耕陶, 魏怀玲, 宋振玉. 联苯双酯对小鼠肝损伤保护作用的进一步研究J. 药学学报, 1982, 17(2): 101-106.
LIU Geng-tao, WEI Huai-ling , SONG Zhen-yu (Chen-yu Sung), . FURTHER STUDIES ON THE PROTECTIVE ACTION OF BIPHENYL DIMETHYL-DICARBOXYLATE (BDD) AGAINST EXPERIMENTAL LIVER INJURY IN MICEJ. Acta Pharmaceutica Sinica, 1982, 17(2): 101-106.
Citation: LIU Geng-tao, WEI Huai-ling , SONG Zhen-yu (Chen-yu Sung), . FURTHER STUDIES ON THE PROTECTIVE ACTION OF BIPHENYL DIMETHYL-DICARBOXYLATE (BDD) AGAINST EXPERIMENTAL LIVER INJURY IN MICEJ. Acta Pharmaceutica Sinica, 1982, 17(2): 101-106.

联苯双酯对小鼠肝损伤保护作用的进一步研究

FURTHER STUDIES ON THE PROTECTIVE ACTION OF BIPHENYL DIMETHYL-DICARBOXYLATE (BDD) AGAINST EXPERIMENTAL LIVER INJURY IN MICE

  • 摘要: 本研究证明:联苯双酯不仅能降低四氯化碳引起的小鼠血清谷丙转氨酶(以下简称SGPT)水平升高,对肝脏病理损害亦有明显的保护作用。此外,还发现联苯双酯能使正常小鼠、四氯化碳肝损伤小鼠及强的松龙处理的小鼠肝组织中GPT降低,但对谷草转氨酶(GOT)及醛缩酶活性无明显影响。在使正常小鼠肝脏GPT活性明显降低时,心脏GPT活性无明显变化。联苯双酯对四氯化碳引起的小鼠SGPT升高的降低作用似非直接抑制血清及肝组织中的GPT活性,或促进血液中GPT的消失。

     

    Abstract: In a previous paper, the SGPT-lowering action of BDD in mice intoxicated with CCl4 or thioacetamide as well as in prednisolone treated mice was reported. The present data indicate that BDD also has significant protective action against liver lesions induced by CCl4 in mice. In addition, BDD was found to decrease the liver GPT (glutamate pyruvate transaminase) activity of normal, CCl4-intoxicated and prednisolone-treated mice. However, no effect of BDD on GOT (glutamic oxaloacetic transaminase) and aldolase activities were observed. Although liver GPT was significantly decreased by BDD, the heart GPT still remained in normal level. Incubation of the serum of mice given BDD with the liver homogenate of CCl4-intoxicated mice at 37℃ for 2 hours in vitro, no decrease of GPT activity of the liver homogenate was obtained. Moreover, no speed up of spontaneous decrease of serum GPT level in mice injected with 5ml/kg of high GPT serum (from CCl4-intoxicated mice) by BDD was found. Therefore, it seems that the SGPT-lowering action of BDD is not due to direct inhibition of serum and liver GPT activities or to the increase of spontaneous disappearence of GPT from mouse blood circulation. The exact mechanism of the protective action of BDD against liver injury in animal remains to be elucidated.

     

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