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Radix Bupleuri is a hepatoprotective traditional Chinese medicine (TCM) usedfor thousands of years in clinical, which was reported to be linked with liverdamage. Previous studies have revealed that saikosaponins are the major typesof components that contribute to the hepatotoxicity of Radix Bupleuri. Howeverthe underlying molecular mechanism is far from being understood. In order toclarify whether these structural analogues exert toxicity effects through thesame molecular targets, a systematic comparison study was done in this paper.The effects of SSa, b2, c, and d on isolated rat liver mitochondria and humanhepatocyte L02 cells were explored, respectively. The collective resultsindicated that although saikosaponins share the similar structures but theyhave quite different mechanisms. SSb2 and SSd showed most serious damage on thefunction of mitochondria and survival rate of cell, respectively. SSb2 couldcause mitochondrial permeability transition pore (mPTP) opening and collapse ofmitochondrial membrane potential ({\Delta}{\Psi}m) by impairing themitochondrial respiratory chain complex III. While SSd destroyed plasmamembrane and led to the release of lactate dehydrogenase (LDH) mainly throughactivating caspase-1. Furthermore, the combine index (CI) demonstrated that thecombined hepatotoxicity of SSb2 and SSd could be additive. This finding mightyield more in depth understanding of hepatotoxicity of Radix Bupleuri possessmany different saikosaponins.

Saikosaponins with similar structures but different mechanisms lead to combined hepatotoxicity