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[Objective]To investigate the effects of saikosaponin a(SSa) of RADIX BUPLEURI on the proliferation of human normal liver cell L-02 and its mechanism,and to provide theoretical basis for clinical application of RADIX BUPLEURI. [Methods]Morphological changes were observed and MTT assay was performed to research the toxicity effects of SSa on human liver cell L-02 in different time periods and doses. DNA ladder analysis and Annexin V /PI double staining were both used to detect if cell apoptosis was induced. The contents of SOD,MDA and LDH in supernatant were detected to further research the mechanism of hepatotoxicity induced by SSa. [Results] SSa of different concentrations were all dose dependent to cytotoxicity,but had no relationship with administration time. IC50 values of SSa after administration for 24 and 48 h were 5. 47 and 5. 22 μmol /L,respectively. Annexin V /PI double staining could not detect the early apoptotic cells. Detection results of cell culture liquid showed that SOD activity reduced,while MDA and LDH contents enhanced. [Conclusions] The mechanism of hepatotoxicity in vitro of SSa was not apoptosis induction,but oxidative injury of human liver cell. SSa reduced the activity of SOD,which resulted in cellular membrane injury and finally caused cytotoxicity.
[Objective] To investigate the effects of saikosaponin a (SSa) of RADIX BUPLEURI on the proliferation of human normal liver cell L-02 and its mechanism, and to provide theoretical basis for clinical application of RADIX BUPLEURI. [Methods] Morphological changes were analyzed and MTT assay was performed to research the toxicity effects of SSa on human liver cell L-02 in different time periods and doses. DNA ladder analysis and Annexin V / PI double staining were both used to detect if cell apoptosis was induced. The contents of SOD, MDA and LDH in supernatant were detected to further research the mechanism of hepatotoxicity induced by SSa. [Results] SSa of different concentrations were all dose dependent to cytotoxicity, but had no relationship with administration time. IC50 values of SSa after administration for 24 and 48 h were 5. 47 and 5. 22 μmol / L, respectively. Annexin V / PI double staining could not detect the early apoptotic cells. Detection results of cell culture liquid showed that that SOD activity reduced, while MDA and LDH contents enhanced. [Conclusions] The mechanism of hepatotoxicity in vitro in SSa was not apoptosis induction, but oxidative injury of human liver cell. SSa reduced the activity of SOD, which resulted in cellular membrane injury and finally caused cytotoxicity.