Peptide T8 isolated from yak milk residue ameliorates H2O2-induced oxidative stress through Nrf2 signaling pathway in HUVEC cells

Abstract

This study was aimed to explore the anti-oxidative effect of active peptide (T8) isolated from yak milk residue on H 2 O 2 -induced damage in HUVEC cells. The results showed that peptide T8 increased superoxide dismutase (SOD) and glutathione reductase (GR) activities while decreased malondialdehyde (MDA) content and ROS of HUVEC cells in the H 2 O 2 -induced damage model. Flow cytometry assays showed that peptide T8 reduced H 2 O 2 -induced cell apoptosis. The protein expression levels of PARP and cleaved-Caspase 9 was increased by Western blot analysis in the H 2 O 2 -induced HUVEC cells. The ratio of Bax/Bcl-2 was increased, suggesting peptide T8 inhibits H 2 O 2 -induced in mitochondrial-dependant death. The protein expression levels of p-Nrf2 was increased in HUVEC cells and the expressions of Nrf2 target genes Keap1, Nrf2, HO-1 and NQO1 were modulated by peptide T8 treatments. Blocking Nrf2 activation by inhibitor ML385, the protective effect of peptide T8 on the H 2 O 2 -induced injury was partially reversed. Our results indicate that peptide T8 ameliorate H 2 O 2 -induced oxidative stress via Nrf2 pathway in HUVEC cells. • The strong antioxidative peptide T8 was isolated from yak milk residue. • Peptide T8 reduced H 2 O 2 -induced damage in HUVEC cells. • Peptide T8 regulated antioxidation-related gene expressions via Nrf2 pathway.