Solanine Induced ROS Production Promote HepG2Cell Apoptosis

Background:Solanine has been considered as anti-tumor therapy during these years, also liver carcinoma bring much more damage to people especially Chinese. The role of solanine to liver carcinoma and detailed molecular mechanism of this drug to liver carcinoma remains unknown.Objectives:To observe the key role of solanine to liver carcinoma and to explore the detailed molecular mechanism of this process.Methods:Using different ROS probes including cytosol and mitochondria, to detect the volume of ROS production both in cytosol and mitochondria when pretreat solanine or not with FACS; Also, detect the apoptosis related protein ASK1and TBP-2, and proliferation related protein TRX2, using western blot when challenged with solanine in HepG2cells; Finally, acounting the cell number in solanine pretreat group, negative control (untreat) and postive control(camptothecin) individually, observe the cell morphology of all the group mentioned above.Results:ROS probe DCFDA and DHR123can detect productive ROS (H2O2and OH-) both in cytosol and mitochondria with pretreat solanine as compared with negative control (untreated group)(p<0.05), whereas superoxide specific probe DHE and MITSOX can not detect the ROS in the same system. Western bloting found solanine up-regulated ASK1and TBP-2level, inhibit TRX2expression. The accounting experiments found that solanine significantly decreased the cell number compared with untreated group, also the morphology of HepG2cell changed much of the experimental group.Conclusions:Solanine can induced ROS production, mainly H2O2and OH-, both in mitochondria dependent and mitochondria independent pattern in HepG2cell, also induce apoptosis protein activation, which promote HepG2cell apoptosis with solanine challenge.