Abstract
Specific mechanisms underlying cardioprotective and anti-inflammatory effects of flavonoids remain unclear. The effects of two flavonoids—hesperidin and naringin—on endothelial nitric oxide synthase (eNOS) induction in human umbilical vein endothelial cells (HUVECs) were investigated here, and possible underlying molecular mechanisms using high glucose (HG) concentrations were examined. The flavonoids' effects on nitric oxide (NO) production and Ser-1177 and Thr-495 phosphorylation with or without mitogen-activated protein kinase (MAPK) signalling pathway inhibitors were determined. HG decreased eNOS mRNA and protein levels while pre-treatment with both flavonoids drastically increased the levels dose- and time-dependently, in HUVECs. Furthermore, HG altered eNOS phosphorylation at Ser1177 and Thr495. Naringin phosphorylated Ser1177 via the p-38 pathway and dephosphorylated Thr495 via the mitogen-activated protein kinase kinase (MEK) and c-Jun N-terminal kinase (JNK) pathways. Hesperidin phosphorylated Ser1177 via the MEK pathway and dephosphorylated Thr495 via the p-38 and JNK pathways. Thus, hesperidin and naringin regulate HG-induced eNOS expression via the MAPK signalling pathway.
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