Curcumin Promotes the Proliferation, Migration, and Angiogenesis of HUVECs to Improve Atherosclerosis through the Wnt/β-Catenin Pathway

Abstract

Background: Atherosclerosis is a chronic inflammatory disease that leads to ischemic cerebrovascular and cardiovascular diseases. Curcumin, known for its anti-inflammatory properties, may influence the development of atherosclerosis. This study aims to elucidate the effects of curcumin and its mechanisms on atherosclerosis progression. Methods: The proliferative ability, the angiogenesis capacity, and cell migration rate were assessed using cell counting kit-8 (CCK-8), 5-ethynyl-29-deoxyuridine (EdU), tube formation assays, and wound healing, respectively. Furthermore, the protein expression levels of proliferating cell nuclear antigen (PCNA), glycogen synthase kinase 3β (GSK3β), p-GSK3β, β-catenin, and c-myc were determined utilizing western blot analysis. Results: Oxidized low-density lipoprotein (ox-LDL) significantly triggered cell damage by inhibiting cell proliferation, reducing the migration rate, and angiogenesis capacity in human umbilical vein endothelial cells (HUVECs) (p < 0.05). Curcumin treatment significantly alleviated ox-LDL-induced HUVECs injury (p < 0.05), as evidenced by elevating the proliferative ability (p < 0.05), cell migration (p < 0.05), and angiogenesis (p < 0.05). Moreover, the Wnt/β-catenin pathway was substantially boosted following ox-LDL treatment (p < 0.05), which was suppressed by curcumin (p < 0.05). Additionally, SKL2001 significantly increased the levels of β-catenin and c-myc (p < 0.05). The inhibitory effects of curcumin treatment on the Wnt/β-catenin signaling pathway were reduced by SKL2001 (p < 0.05). Furthermore, the promoting effects of curcumin on ox-LDL-induced cell damage were hampered following SKL2001 treatment in HUVECs (p < 0.05). Conclusion: Curcumin elevated cell proliferation, migration, and angiogenesis of HUVECs to inhibit the development of atherosclerosis through inactivating the Wnt/β-catenin pathway.