Frontiers in pharmacology · 2026
β-sitosterol ameliorates myocardial infarction injury via modulating the NF-κB and necroptosis signaling pathways.
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Xu Jia-Jia, Chen Min-Wei, Lai Long-Zhen, Xiao Di, Jiang Shu-Yan, Lin Jun-Xin, Zhang Zheng-Hao, Shan Zhong-Gui
Аннотация
INTRODUCTION: Acute myocardial infarction (MI) is a leading global cause of morbidity and mortality, where inflammatory response and programmed cell death (PCD) are critical in disease progression. β-sitosterol (β-SITO), a phytosterol with known cardioprotective effects, has been implicated in cardiovascular diseases, but its specific role and mechanisms in MI remain underexplored.
METHODS: This study employed both in vivo and in vitro models. Male C57BL/6J mice with MI were used to evaluate the effects of β-SITO treatment. Cardiac function was assessed via echocardiography, infarct size and fibrosis were analyzed histologically. In vitro, cardiomyocyte viability under hypoxia and TGF-β-induced cardiac fibroblast activation were examined. Mechanistic insights were gained through transcriptomic profiling, molecular docking studies, and validation by Western blotting.
RESULTS: β-SITO treatment significantly reduced myocardial infarct size, alleviated cardiac fibrosis, and improved cardiac function in MI mice. In vitro, it enhanced cardiomyocyte viability under hypoxia and inhibited TGF-β-induced fibroblast activation. Transcriptomic analysis revealed that β-SITO modulated pathways related to immune-inflammatory responses, NF-κB, and necroptosis signaling. Molecular docking confirmed its strong binding affinity to key components of these pathways. Western blotting validated the inhibition of NF-κB activation and necroptosis in both hypoxic cardiomyocytes and MI mouse heart tissue.
CONCLUSION: β-SITO demonstrates significant therapeutic potential for improving post-MI recovery. Its cardioprotective effects are likely mediated through the modulation of NF-κB and necroptosis signaling pathways, highlighting it as a promising candidate for MI treatment.
METHODS: This study employed both in vivo and in vitro models. Male C57BL/6J mice with MI were used to evaluate the effects of β-SITO treatment. Cardiac function was assessed via echocardiography, infarct size and fibrosis were analyzed histologically. In vitro, cardiomyocyte viability under hypoxia and TGF-β-induced cardiac fibroblast activation were examined. Mechanistic insights were gained through transcriptomic profiling, molecular docking studies, and validation by Western blotting.
RESULTS: β-SITO treatment significantly reduced myocardial infarct size, alleviated cardiac fibrosis, and improved cardiac function in MI mice. In vitro, it enhanced cardiomyocyte viability under hypoxia and inhibited TGF-β-induced fibroblast activation. Transcriptomic analysis revealed that β-SITO modulated pathways related to immune-inflammatory responses, NF-κB, and necroptosis signaling. Molecular docking confirmed its strong binding affinity to key components of these pathways. Western blotting validated the inhibition of NF-κB activation and necroptosis in both hypoxic cardiomyocytes and MI mouse heart tissue.
CONCLUSION: β-SITO demonstrates significant therapeutic potential for improving post-MI recovery. Its cardioprotective effects are likely mediated through the modulation of NF-κB and necroptosis signaling pathways, highlighting it as a promising candidate for MI treatment.