期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 70, 期 36, 页码 -出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.2c04045
关键词
hesperidin; Mas receptor; TRPV1; nitric oxide; HUVEC
资金
- JSPS KAKENHI [JP21H04863]
- 2021 Nagasaki Strategy Project Study
This study investigated the mechanism of vasorelaxant Mas receptor (MasR) expression elevated by hesperidin in spontaneously hypertensive rats in human umbilical vein endothelial cells (HUVECs). The results showed that hesperidin may stimulate TRPV1-mediated cascades, leading to the activation of two signaling axes, CaMKII/p38 MAPK/MasR expression and CaMKII/eNOS/NO production in HUVECs.
Here, the mechanism of vasorelaxant Mas receptor (MasR) expression elevated by hesperidin in spontaneously hypertensive rats was investigated in human umbilical vein endothelial cells (HUVECs). HUVECs were cultured with 1 mu M hesperidin for 2 h, following the measurements of nitric oxide (NO) production and vasomotor-related receptors' expression. Hesperidin significantly promoted NO production (224.1 +/- 18.3%, P < 0.01 vs control) in the HUVECs. Only the MasR expression was upregulated (141.2 +/- 12.5%, P < 0.05 vs control), whereas a MasR antagonist did not alter the hesperidin-induced NO production. When a transient receptor potential vanilloid 1 (TRPV1) was knocked down by silencing RNA or Ca2+/calmodulindependent kinase II (CaMKII) and p38 mitogen-activated protein kinase (p38 MAPK) were inhibited, the increased MasR expression by hesperidin was abrogated. The inhibitions of CaMKII and endothelial NO synthase (eNOS) abolished the hesperidininduced NO production. The structure-activity relationship analysis of flavonoids demonstrated that the B ring of the twisted flavonoid skeleton with a hydroxy group at the 3 ' position was a crucial factor for TRPV1 stimulation. Taken together, it was demonstrated that hesperidin may stimulate TRPV1-mediated cascades, leading to the activation of two signaling axes, CaMKII/p38 MAPK/MasR expression and CaMKII/eNOS/NO production in HUVECs.
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