Inflammation and fibrosis are closely connected mechanisms that contribute to the advancement of chronic diseases. Persistent inflammatory responses stimulate fibroblast activity, accumulation of extracellular matrix, and tissue fibrosis, resulting in organ dysfunction and related disorders.The modulation of these pathways offers a promising approach for therapeutic intervention, particularly in malignancies where inflammation-driven fibrosis supports tumor growth and survival. This study investigated the regulatory effects of Eptifibatide, a cyclic heptapeptide and GPIIb/IIIa receptor antagonist, on cell proliferation, apoptosis, and inflammatory signaling.The regulatory effects of Eptifibatide on cell growth and apoptosis were evaluated by MTT and flow cytometric methods. The anti-proliferative potential of Eptifibatide was assessed in a murine model of breast cancer, and its regulatory effects on pro-fibrotic and Pro-inflammatory cytokines were also investigated using real-time PCR and ELISA methods. Eptifibatide induced cell cycle arrest and apoptosis by elevating reactive oxygen species (ROS) levels and upregulating the expression of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β. Our findings demonstrate that Eptifibatide can inhibit cell growth and proliferation through inducing oxidative stress and inflammatory responses in cell and animal models of breast cancer.

Keywords