Pik3cb Antagonizes LPS/ATP-Induced Inflammatory Activation in Cardiomyocytes by Inhibiting the PI3K/AKT/NF-<b>κ</b>B/NLRP3 Signaling Axis

Objectives: PI3K plays a pivotal role in the inflammatory response by modulating the production and release of inflammatory factors. Pik3cb is one of the subunits of PI3K, and its specific role in myocardium inflammation remains unelucidated. This study aimed to investigate the role of Pik3cb in the inflammatory response and to elucidate the underlying mechanism. Methods: An inflammation model was established using H9c2 cells treated with LPS and ATP, and Pik3cb expression was evaluated in this model system. Subsequently, an overexpression model was constructed by transfecting cells with a Pik3cb overexpression plasmid, after which the effects of Pik3cb overexpression on the PI3K/AKT and NF-κB/NLRP3 inflammatory signaling pathways were assessed. Results: These analyses revealed that the expression and distribution of Pik3cb were significantly reduced in the LPS/ATP-induced cellular inflammation model group, whereas plasmid-mediated overexpression of Pik3cb significantly inhibited the activation of the PI3K/AKT signaling pathway in response to LPS/ATP stimulation. Additionally, the LPS/ATP-induced activation of the NF-κB/NLRP3 axis was significantly inhibited following Pik3cb overexpression. Conclusion: This study demonstrates that Pik3cb acts as a negative regulator of LPS/ATP-induced inflammation in cardiomyocytes, exerting anti-inflammatory effects by inhibiting the PI3K/AKT/NF-κB/NLRP3 signaling axis. These findings provide a potential therapeutic target for the treatment of myocardial inflammation.