Shenling Jiangzhi Formula alleviates atherosclerosis in ApoE-/- mice by inhibiting vascular inflammation via `NF-κB`/`NLRP3` pathway

Atherosclerosis (AS) is a chronic inflammatory disease characterized by plaque buildup in arteries, leading to cardiovascular events. Current treatments often focus on lipid lowering, but addressing the underlying vascular inflammation remains a critical challenge. Traditional Chinese Medicine (TCM) offers multi-component formulas like Shenling Jiangzhi Formula (SJF), which is clinically used for AS, aligning with TCM concepts of "blood stasis" and "vascular impediment" linked to spleen deficiency and dampness. However, the precise molecular mechanisms by which SJF exerts its anti-atherosclerotic effects, particularly its influence on key inflammatory pathways like NF-κB and NLRP3, have remained largely uncharacterized.

Researchers investigated Shenling Jiangzhi Formula (SJF) using UPLC-Q-Exactive Orbitrap MS/MS to identify 313 chemical components. Network pharmacology and molecular docking were employed to predict core targets and active components against AS. An ApoE-/- mouse model of AS was established using a high-fat diet combined with an intermittent water environment (sleep deprivation). Rosuvastatin served as a positive control. ELISA was used to measure serum lipids (TC, TG, LDL-C, HDL-C), inflammatory cytokines (hs-CRP, IL-1β, IL-6, IL-18, NF-κB, MCP-1), and other markers (Hb, TMAO, Orexin A). HE staining and Oil Red O staining assessed cell morphology and aortic plaque area. Western blotting quantified aortic protein expression of IL-1β, IL-18, NF-κB p65, p-NF-κB p65, NLRP3, Caspase-1, cleaved Caspase-1 (p20), and ASC.

The study identified a total of 313 chemical components within Shenling Jiangzhi Formula (SJF) using UPLC-Q-Exactive Orbitrap MS/MS technology. Network pharmacology and molecular docking predicted that SJF targets key pathways relevant to atherosclerosis. While the abstract states the aim was to observe regulatory effects on plaque formation and inflammatory response, and to clarify anti-AS mechanisms, the provided 'RESULTS' section of the abstract is incomplete, only stating the number of identified chemical components. Specific quantitative data regarding plaque reduction, changes in inflammatory markers, or direct modulation of the NF-κB/NLRP3 pathway were not detailed in the provided abstract snippet.