基于FOXO1介导的抗氧化通路探讨小檗碱联合肉桂醛干预主动脉内皮细胞炎症的分子机制OA

Objective To investigate the molecular mechanisms by which berberine combined with cinnamaldehyde ameliorates inflammation in aortic endothelial cells based on FOXO1/CAT/SOD2 pathway.Methods A human aortic endothelial cell(HAEC)inflammatory model was established by treating cells with 100 μg/mL lipopolysaccharide(LPS)for 24 h.Cells were subsequently treated with berberine,cinnamaldehyde,or a combination of both(berberine+cinnamaldehyde),at a final concentration of 5 μmol/L for 24 h.Cell viability was assessed using the CCK-8 assay;apoptosis rates were determined by flow cytometry;immunofluorescence staining was employed to evaluate expression levels of von Willebrand factor(vWF)and endothelial nitric oxide synthase(eNOS);Western blot was utilized to assess protein expression levels of forkhead box O1(FOXO1)and its downstream antioxidant enzymes catalase(CAT)and superoxide dismutase 2(SOD2).Results Compared with the LPS-induced group,both individual and combined administration of berberine and cinnamaldehyde significantly increased HAEC viability(P<0.05,P<0.01)and reduced the proportion of apoptotic cells(P<0.05,P<0.01);Concurrently,drug intervention markedly downregulated expression of the inflammatory marker vWF whilst upregulating levels of the endothelial protective factor eNOS.Regarding molecular mechanisms,the individual and combination groups exhibited significantly elevated FOXO1 expression(P<0.01)and increased levels of downstream antioxidant proteins CAT and SOD2(P<0.01),with the combination group demonstrating superior efficacy to monotherapy.Conclusion Berberine combined with cinnamaldehyde effectively counteracts LPS-induced inflammation in HAEC,potentially through upregulating the FOXO1/CAT/SOD2 pathway.This suggests the combination possesses potential vascular endothelial protective effects.