Resibufogenin protects against atherosclerosis in ApoE(-/-) mice through blocking NLRP3 inflammasome assembly.

INTRODUCTION: Atherosclerosis (AS), a major cause of cardiovascular diseases, is characterized by lipid accumulation and chronic inflammation within arterial walls. Traditional treatments, such as statins, are often ineffective for many patients, highlighting the need for novel therapeutic strategies. OBJECTIVE: This study explores the potential of Resibufogenin (RBG) as an NLRP3 inflammasome inhibitor for treating AS in ApoE METHODS: We performed experiments encompassing cellular studies, animal model assessments, molecular simulations, and binding assays to assess RBG's impact on the NLRP3 inflammasome, inflammatory cytokine release, and foam cell formation. RESULTS: RBG treatment alleviated AS in ApoE CONCLUSION: RBG effectively inhibits NLRP3 inflammasome activation, reduces pro-inflammatory cytokine release, and decreases formation of foamy macrophages, thereby slowing the progression of AS. Although these findings highlight RBG as a promising therapeutic approach for cardiovascular diseases, further research is necessary to assess its safety and effectiveness in humans and to investigate possible synergistic effects with other treatments.