How a Dietary Anthocyanin Activates Nrf2 in Endothelial Cells

Dissecting the signaling events triggered by C3G under TNF‑α challenge

Endothelial dysfunction is shaped by oxidative and inflammatory stress. This in vitro study examines how the anthocyanin C3G influences antioxidant responses in HUVECs, particularly focusing on Nrf2 activation and MAPK involvement.

Original article: Cyanidin‑3‑O‑glucoside counters the response to TNF‑alpha of endothelial cells by activating Nrf2 pathway, DOI: 10.1002/mnfr.201300102, https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201300102

Q&A Q: What triggers the protective response? A: C3G activates the Nrf2/ARE pathway, boosting antioxidant defenses.

Q: Which signaling pathway is involved? A: ERK1/2 activity is required for Nrf2 nuclear translocation.

Q: What happens if ERK1/2 is inhibited? A: Nrf2 activation is blocked and NF‑κB translocation increases.

Q: Are these effects physiological? A: They are shown in vitro, and further validation is needed.

Key results • C3G prevents oxidative stress in HUVECs. • It enhances cellular antioxidant capacity. • It activates Nrf2/ARE signaling both at baseline and under TNF‑α. • ERK1/2 inhibition abolishes Nrf2 activation and enhances NF‑κB p65 nuclear translocation.