Puerarin protects endothelial progenitor cells from damage of angiotensin II via activation of ERK1/2‑Nrf2 signaling pathway.

Endothelial progenitor cell (EPC) dysfunction is associated with the formation of carotid atherosclerosis. It has been demonstrated that angiotensin II (Ang II) may impair the function of EPCs and puerarin, a natural product, possesses cardiovascular protective effects against oxidative stress and inflammation. Therefore, the present study aimed to investigate the beneficial effects of puerarin in Ang II‑induced EPC injury, and to elucidate the underlying mechanisms. Treatment with Ang II suppressed EPC proliferation and migration, increased the expression of the senescence marker β‑galactosidase, and the adhesion molecules intracellular adhesion molecule‑1 and vascular cell adhesion molecule‑1. However, the above effects were markedly alleviated by treatment with puerarin in a dose‑dependent manner (1, 10 and 100 µM). In addition, Ang II significantly increased reactive oxygen species production and the levels of the inflammatory cytokine tumor necrosis factor‑α and interleukin‑6. Notably, these effects were reversed by puerarin. However, it was identified that the impaired EPC functions were due to inhibition of the phosphorylation of extracellular signal‑regulated kinase 1 and 2 (ERK1/2) and the degradation of nuclear factor erythroid 2 like 2 (Nrf2), and treatment with puerarin activated the ERK1/2‑Nrf2 signaling pathway. The results of the present study indicated that puerarin protected Ang II‑induced EPC dysfunction via activation of the ERK1/2‑Nrf2 signaling pathway.