Abstract
Background/PurposePorphyromonas gingivalis (P. gingivalis) has been shown to induce apoptosis in endothelial cells and contribute to the progression of atherosclerosis. While Polyinosinic-polycytidylic acid (Poly (I:C)) is known to activate the innate immune response against infections, its potential interference with P. gingivalis-induced atherosclerosis remains unclear. This study aimed to elucidate the role and underlying mechanisms of Poly (I:C) in mediating human umbilical vein endothelial cells (HUVECs) apoptosis induced by P. gingivalis. Materials and methodsA mice model of atherosclerosis and a model of P. gingivalis-induced bacteremia were established to investigate the effects of Poly (I:C) on P. gingivalis-induced apoptosis in the aortic root, as well as the expression levels of apoptosis-related proteins including Caspase 3, Caspase 9, Bax, and Bcl-2. Subsequently, HUVECs were cultured in vitro to compare cell apoptosis and the expression of these apoptosis-related proteins under stimulation with P. gingivalis, both with and without Poly (I:C) treatment; additionally, the activation status of the JAK/STAT signaling pathway was assessed. ResultsThe administration of Poly (I:C) diminished apoptosis in the aortic root cells of mice, enhanced the expression of the anti-apoptotic protein Bcl-2, and decreased the levels of Bax, Caspase 3 and 9. Furthermore, Poly (I:C) exhibited similar effects on HUVECs cultured in vitro. Additionally, treatment with Poly (I:C) activated the JAK/STAT signaling pathway, while STAT inhibitor was found to attenuate its effects. ConclusionPoly (I:C) attenuated P. gingivalis-induced cellular apoptosis, with the involvement of the JAK/STAT signaling pathway in this mechanism.
Published Version
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