Procyanidin B2 mitigate asthmatic airway remodeling by inhibiting TGF-β1-induced airway smooth muscle proliferation through ROS signaling

Introduction: Asthma is characterized by airway remodeling with increased airway smooth muscle (ASM) mass which contributes significantly to the progressive decline in lung function in asthma patients. Despite advances in therapeutic strategies targeting airway remodeling, their efficacy remains suboptimal. Procyanidin B2, antioxidants derived from grape seeds, have demonstrated potential benefits in the treatment of asthma. However, the role of procyanidin B2 involved in mitigating the process of airway remodeling and the underlying mechanisms remain unclear. Methods: This study investigated the effects of procyanidin B2 on ASM in asthma, with a particular focus on the molecular mechanisms involved. The markers of ASM proliferation and phenotypic switching by procyanidin B2 administration were analyzed, as well as its regulatory influence on key signaling pathways in asthma pathophysiology, to elucidate the underlying mechanism of procyanidin B2 in the control of ASM function. Results: The results showed that procyanidin B2 effectively modulated ASM proliferation and phenotypic switching. Procyanidin B2 inhibited TGF-beta 1-induced proliferation and phenotypic switching of ASM cells by reducing the expression of transformation markers (alpha-SMA, COL1A1). Blocking critical pathways such as MAPK and Akt signaling may be responsible for the suppression of ASM ROS production, which has been implicated in the pathogenesis of asthma remodeling. Conclusion: This study revealed procyanidin B2 as a promising therapeutic option for asthma, highlighting the novel potential of procyanidin B2 in ASM-driven changes in this disease. These findings provide the basis and support for further research on procyanidin B2 intervention as a means to improve clinical outcomes in asthma patients.