Kaempferol protects lipopolysaccharide-induced inflammatory injury in human aortic endothelial cells (HAECs) by regulation of miR-203.

Hypertension is a common public health problem due to its high morbidity and potential risk, which is related to inflammatory actions. Kaempferol (KAE) has anti-inflammation activities. Herein, we explored the effects of KAE on LPS-induced inflammatory injury in human aortic endothelial cells (HAECs). HAECs were treated with KAE before stimulated with LPS or AngII. After miR-203 inhibitor transfection, cell viability and apoptosis were detected by CCK-8 and flow cytometry. The accumulated levels of apoptotic proteins, nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways related proteins, MyD88 and toll-like receptor 4 (TLR4) were both determined by western blot. The concentrations of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were detected by ELISA. Expression of miR-203 was analyzed by qRT-PCR. The target of miR-203 was achieved by luciferase assay. LPS successfully induced inflammatory injury as evidenced by decreasing cell viability, increasing apoptosis, and also increasing IL-6, TNF-α concentrations. The apoptotic proteins p53 and cleaved-Caspase-3 were both upregulated while Bcl-2 was downregulated. Moreover, LPS activated NF-κB and MAPK pathways. However KAE reversed the results led by LPS. KAE increased miR-203 expression in LPS or AngII-disposed HAECs. More experiments revealed that transfection with miR-203 inhibitor impaired the inflammation-alleviating effects of KAE. MyD88 and TLR4 were predicated as a target of miR-203, which might be implicated in the protective functions of KAE on HAECs. KAE exerted the protective impacts on HAECs against inflammatory injury through inactivation of NF-κB and MAPK pathways, as well as upregulation of miR-203.