biostudies-literatureLin YNational Natural Science Foundation of ChinaGuangdong Major Project of Basic and Applied Basic Research1837https://www.ebi.ac.uk/biostudies/studies/S-EPMC9495744biostudies-literatureUnknown11(9)Chelerythrine (CHE) is a majorly harmful isoquinoline alkaloid ingredient in <i>Chelidonium majus</i> that could trigger potential hepatotoxicity, but the pivotal molecular mechanisms remain largely unknown. In the present study, CHE-induced cytotoxicity and the underlying toxic mechanisms were investigated using human HepG2 cells in vitro. Data showed that CHE treatment (at 1.25-10 μM)-induced cytotoxicity in HepG2 cells is dose-dependent. CHE treatment increased the production of ROS and induced oxidative stress in HepG2 cells. Additionally, CHE treatment triggered the loss of mitochondrial membrane potential, decreased the expression of mitochondrial complexes, upregulated the expression of Bax, CytC, and cleaved-PARP1 proteins and the activities of caspase-9 and caspase-3, and downreguAntioxidants (Basel, Switzerland)Chelerythrine-Induced Apoptotic Cell Death in HepG2 Cells Involves the Inhibition of Akt Pathway and the Activation of Oxidative Stress and Mitochondrial Apoptotic Pathway.PMC949574432102724No. 2020B0301030007Shen JDai CJiang HTang SLin YZhang QXie BfalseChelerythrine-Induced Apoptotic Cell Death in HepG2 Cells Involves the Inhibition of Akt Pathway and the Activation of Oxidative Stress and Mitochondrial Apoptotic Pathway.Chelerythrine (CHE) is a majorly harmful isoquinoline alkaloid ingredient in <i>Chelidonium majus</i> that could trigger potential hepatotoxicity, but the pivotal molecular mechanisms remain largely unknown. In the present study, CHE-induced cytotoxicity and the underlying toxic mechanisms were investigated using human HepG2 cells in vitro. Data showed that CHE treatment (at 1.25-10 μM)-induced cytotoxicity in HepG2 cells is dose-dependent. CHE treatment increased the production of ROS and induced oxidative stress in HepG2 cells. Additionally, CHE treatment triggered the loss of mitochondrial membrane potential, decreased the expression of mitochondrial complexes, upregulated the expression of Bax, CytC, and cleaved-PARP1 proteins and the activities of caspase-9 and caspase-3, and downregu2022-01-01T00:00:00Z2022 Sep2025-04-21T16:08:15.446Z2025-02-19T00:42:04.48ZS-EPMC94957443613991110.3390/antiox11091837