Mitochondrial dysfunction and oxidative stress, triggered by angiotensin II (Ang II) overactivation, are key drivers of cardiovascular disease (CVD) progression. This study compares the protective effects of nebivolol, a third-generation β1-adrenergic blocker, and metoprolol, a second-generation β1-adrenergic blocker, on Ang II-induced mitochondrial impairment in H9c2 cardiomyoblasts.
The study evaluated nebivolol and metoprolol’s protective effects against Ang II-induced mitochondrial dysfunction in H9c2 cells. Intracellular reactive oxygen species (ROS) production was measured using 2’,7’-dichlorofluorescein (DCF) fluorescence. Protein and mRNA levels were quantified via Western blotting and real-time PCR, respectively, to assess molecular changes.
Both nebivolol and metoprolol significantly reduced Ang II-induced ROS generation and downregulated the expression of apoptotic (e.g., BNIP3) and proinflammatory genes. However, nebivolol outperformed metoprolol by more effectively suppressing BNIP3, upregulating the antioxidant defense system (e.g., BCL2), and enhancing mitochondrial biogenesis and fusion-related gene expression. These findings indicate nebivolol’s superior ability to restore mitochondrial function and cellular resilience compared to metoprolol.
Both nebivolol and metoprolol effectively mitigate oxidative stress and proinflammatory gene expression in response to Ang II in H9c2 cells. Nevertheless, nebivolol offers enhanced protection by bolstering the antioxidant defense system and improving mitochondrial dynamics, suggesting a potential therapeutic edge in managing Ang II-induced cardiac pathology. These results underscore the importance of considering nebivolol’s unique mechanisms in CVD treatment strategies.
