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Andrographolide Induces ROS-dependent Apoptosis and Suppresses STAT3 Phosphorylation in Primary Effusion Lymphoma
Itnarin Mongkon1,2, Ryusho Kariya1,3, Phorutai Pearngam1,4
1Division of Hematopoiesis, Joint Research Center for Human Retrovirus Infection and Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Background/Aim:
Primary effusion lymphoma (PEL) is a rare and aggressive form of non-Hodgkin lymphoma (NHL) with poor prognosis due to resistance to conventional chemotherapy. Andrographolide (AG), a diterpenoid lactone extracted from Andrographis paniculata, has shown anti-tumor activity in several malignancies, but its effects on PEL are unknown.
Materials And Methods:
PEL cell viability was assessed by MTT assay. Apoptosis was evaluated via Annexin V/PI staining and caspase activation. ROS generation was measured by DCFH-DA staining. Protein expression changes were analyzed by Western blotting. To determine the roles of ROS and caspases, cells were co-treated with a reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) or the pan-caspase inhibitor Q-VD-OPh. AG's in vivo effects were tested in a xenograft mouse model.
Results:
AG inhibited PEL cell proliferation in a dose- and time-dependent manner. Apoptosis was mediated via ROS production and caspase activation. STAT3 phosphorylation was suppressed in a ROS-dependent manner. In vivo, AG (500 mg/kg/day, oral gavage) significantly reduced tumor burden without observable toxicity.
Conclusion:
AG exerts anti-tumor effects against PEL by inducing ROS-dependent apoptosis and suppressing STAT3 signaling. These findings suggest that AG may serve as a promising therapeutic agent for PEL.
