Data-Independent Acquisition-Based Quantitative Proteomic Analysis Reveals the Protective Effect of Apigenin on Palmitate-Induced Lipotoxicity in Human Aortic Endothelial Cells.

The ingestion of excessive free fatty acid could induce lipotoxicity in tissues and then lead to the initiation of many metabolism diseases. In this work, the protective effect of apigenin on palmitate-induced lipotoxicity in human aortic endothelial cells (HAEC) was investigated. Compared with 150 μM palmitate treatment alone, pretreatment with 10 μM apigenin for 6 h significantly increased the cell viability from 71.55 ± 3.62 to 91.06 ± 4.30% and improved mitochondrial membrane potential to the normal level (101.62 ± 11.72% of control). In addition, the production of nitric oxide was markedly elevated by apigenin cotreatment from 7.10 ± 3.95 to 94.20 ± 21.86%. The data-independent acquisition-based proteomic approach was used to study the protective mechanism, and the results revealed that 242 proteins were differently expressed in cells treated with palmitate and 93 proteins were reversed after apigenin supplementation. Apigenin realized its protective function mainly via regulating pathways such as IL-17, TNF, Fox O, cell adhesion, and endoplasmic reticulum protein processing. Collectively, these data demonstrated that apigenin supplement may serve as an alternative nutritional intervention to protect HAEC against lipotoxicity.