Naringenin attenuates inflammation and apoptosis in lipopolysaccharide-induced H9c2 cardiomyocytes

Naringenin, a natural flavonoid, has various pharmacological effects. However, the function of naringenin in cardiac inflammation remains unclear. This study investigated whether naringenin alleviates cardiac inflammatory induced by lipopolysaccharide (LPS). Naringenin's regulatory targets in inflammation and apoptosis were investigated using network pharmacology and molecular docking. LPS activated H9c2 cardiomyocytes, which were then treated with naringenin. Naringenin (20 or 40 μM) reduced the expression of cytokine induced by LPS (P < 0.05). In LPS-induced cells treated with naringenin (20 μM), the nuclear translocation of p65 was inhibited, concomitantly with a significant reduction in IκBα degradation. TUNEL staining revealed that naringenin (20 μM) significantly reduced apoptosis triggered by LPS (P < 0.05). Naringenin (20 μM) also significantly decreased the expression level of Bax and cleaved-caspase 3, and significantly elevated Bcl-2 expression. Naringenin may be able to attenuate H9c2 cardiomyocyte inflammation and apoptosis induced by LPS.