Kaempferol alleviates ox-LDL-induced apoptosis by up-regulation of miR-26a-5p via inhibiting TLR4/NF-κB pathway in human endothelial cells - 13/11/18
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Abstract |
Background |
Oxidized low-density lipoprotein (ox-LDL) has been well-documented to induce endothelial cell (EC) apoptosis and contribute to the progression of atherosclerosis. Kaempferol was reported to alleviate ox-LDL-induced apoptosis of human umbilical vein endothelial cells. However, the detailed mechanism by which kaempferol alleviated ox-LDL-induced EC apoptosis remains largely elusive.
Methods |
The expression of miR-26a-5p in human aortic endothelial cells (HAECs) treated with either ox-LDL alone or in combination with kaempferol was detected by qRT-PCR. Cell viability and apoptosis were assessed by MTT assay and flow cytometry, respectively. The interaction between miR-26a-5p and toll-like receptor 4 (TLR4) mRNA was examined by luciferase reporter assay. The protein levels of TLR4, phosphorylated-p65, p65, phosphorylated-IκBα and IκBα were determined by western blot.
Results |
Kaempferol upregulated miR-26a-5p expression in ox-LDL-stimulated HAECs. Moreover, kaempferol alleviated ox-LDL-induced apoptosis in HAECs by upregulating miR-26a-5p. Additionally, TLR4 mRNA was identified as a target of miR-26a-5p in ox-LDL-treated HAECs. TLR4 overexpression partially counteracted the anti-apoptotic role of miR-26a-5p in ox-LDL-treated HAECs. Furthermore, kaempferol inactivated the TLR4/nuclear factor kappa B (NF-κB) signaling pathway in ox-LDL-treated HAECs by upregulating miR-26a-5p.
Conclusion |
Kaempferol alleviated ox-LDL-induced apoptosis in HAECs by upregulating miR-26a-5p via inactivation of the TLR4/NF-κB signaling pathway, shedding light on the molecular mechanism by which kaempferol alleviated ox-LDL-induced EC apoptosis.
Le texte complet de cet article est disponible en PDF.Keywords : Kaempferol, ox-LDL, miR-26a-5p, The TLR4/NF-κB signaling pathway, HAECs, Atherosclerosis
Plan
Vol 108
P. 1783-1789 - décembre 2018 Retour au numéro
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