The aim of the present study was to explore the protective effects of raspberry and its bioactive compound cyanidin 3-O-glucoside against H2O2-induced oxidative stress in HepG2 cells. We established a model of oxidative stress in HepG2 cells induced by H2O2 and examined the protein expression of Keap1/Nrf2. The antioxidant activity of raspberry extract was carried out measuring the level of reactive oxygen species (ROS), and the changes of phase II detoxification elements such as GSH level and CAT activity. Also the expression of proteins related to the Keap1/Nrf2 signaling was tested. The results revealed that raspberry extract significantly reduced the ROS levels in oxidative injured cells, increased GSH content and CAT activity, and activated the expression of proteins Keap1, Nrf2, HO-1, NQO1, and γ-GCS. These results taken together indicated that raspberry treatment could ameliorate H2O2-induced oxidative stress in HepG2 cells via Keap1/Nrf2 pathway.
Protective effects of raspberry on the oxidative damage in HepG2 cells through Keap1/Nrf2-dependent signaling pathway
Filosa R.;
2019-01-01
Abstract
The aim of the present study was to explore the protective effects of raspberry and its bioactive compound cyanidin 3-O-glucoside against H2O2-induced oxidative stress in HepG2 cells. We established a model of oxidative stress in HepG2 cells induced by H2O2 and examined the protein expression of Keap1/Nrf2. The antioxidant activity of raspberry extract was carried out measuring the level of reactive oxygen species (ROS), and the changes of phase II detoxification elements such as GSH level and CAT activity. Also the expression of proteins related to the Keap1/Nrf2 signaling was tested. The results revealed that raspberry extract significantly reduced the ROS levels in oxidative injured cells, increased GSH content and CAT activity, and activated the expression of proteins Keap1, Nrf2, HO-1, NQO1, and γ-GCS. These results taken together indicated that raspberry treatment could ameliorate H2O2-induced oxidative stress in HepG2 cells via Keap1/Nrf2 pathway.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
