Protective effect of Phikud Navakot extract against hydrogen peroxide-induced oxidative stress in HepG2 cells
Abstract
Objective: The purpose of the study is to evaluate the hepatoprotective effects of Phikud Navakot (PN) extract against H2O2-induced oxidative stress in HepG2 cells.
Methods: The cells were treated with concentrations of PN up to 1 mg/ml prior to incubation with H2O2. Cell viability and ROS generation were assessed by MTT and DCFH-DA assays, respectively. Oxidative defense mechanisms were investigated by measuring glutathione levels and activities of antioxidant enzymes. Expression of Nrf2 and HO-1 proteins were investigated by western blot analyses.
Results: The results showed that PN extract at concentrations of 0.001- 0.1 mg/ml significantly improved cell viability and prevented ROS generation induced by H2O2 in HepG2 cells. The extract also increased the activities of antioxidant enzymes (CAT, GPx, GR and SOD), total GSH, GSH and the GSH/GSSG ratio, but decreased GSSG. Pretreatment with PN prevented the decreases in Nrf2 and HO-1 protein levels caused by H2O2-induced oxidative stress.
Conclusion: This study highlights the hepatoprotective effect of PN against H2O2-induced oxidative stress and the associated mechanisms.
Objective: The purpose of the study is to evaluate the hepatoprotective effects of Phikud Navakot (PN) extract against H2O2-induced oxidative stress in HepG2 cells.
Methods: The cells were treated with concentrations of PN up to 1 mg/ml prior to incubation with H2O2. Cell viability and ROS generation were assessed by MTT and DCFH-DA assays, respectively. Oxidative defense mechanisms were investigated by measuring glutathione levels and activities of antioxidant enzymes. Expression of Nrf2 and HO-1 proteins were investigated by western blot analyses.
Results: The results showed that PN extract at concentrations of 0.001- 0.1 mg/ml significantly improved cell viability and prevented ROS generation induced by H2O2 in HepG2 cells. The extract also increased the activities of antioxidant enzymes (CAT, GPx, GR and SOD), total GSH, GSH and the GSH/GSSG ratio, but decreased GSSG. Pretreatment with PN prevented the decreases in Nrf2 and HO-1 protein levels caused by H2O2-induced oxidative stress.
Conclusion: This study highlights the hepatoprotective effect of PN against H2O2-induced oxidative stress and the associated mechanisms.
Methods: The cells were treated with concentrations of PN up to 1 mg/ml prior to incubation with H2O2. Cell viability and ROS generation were assessed by MTT and DCFH-DA assays, respectively. Oxidative defense mechanisms were investigated by measuring glutathione levels and activities of antioxidant enzymes. Expression of Nrf2 and HO-1 proteins were investigated by western blot analyses.
Results: The results showed that PN extract at concentrations of 0.001- 0.1 mg/ml significantly improved cell viability and prevented ROS generation induced by H2O2 in HepG2 cells. The extract also increased the activities of antioxidant enzymes (CAT, GPx, GR and SOD), total GSH, GSH and the GSH/GSSG ratio, but decreased GSSG. Pretreatment with PN prevented the decreases in Nrf2 and HO-1 protein levels caused by H2O2-induced oxidative stress.
Conclusion: This study highlights the hepatoprotective effect of PN against H2O2-induced oxidative stress and the associated mechanisms.
Objective: The purpose of the study is to evaluate the hepatoprotective effects of Phikud Navakot (PN) extract against H2O2-induced oxidative stress in HepG2 cells.
Methods: The cells were treated with concentrations of PN up to 1 mg/ml prior to incubation with H2O2. Cell viability and ROS generation were assessed by MTT and DCFH-DA assays, respectively. Oxidative defense mechanisms were investigated by measuring glutathione levels and activities of antioxidant enzymes. Expression of Nrf2 and HO-1 proteins were investigated by western blot analyses.
Results: The results showed that PN extract at concentrations of 0.001- 0.1 mg/ml significantly improved cell viability and prevented ROS generation induced by H2O2 in HepG2 cells. The extract also increased the activities of antioxidant enzymes (CAT, GPx, GR and SOD), total GSH, GSH and the GSH/GSSG ratio, but decreased GSSG. Pretreatment with PN prevented the decreases in Nrf2 and HO-1 protein levels caused by H2O2-induced oxidative stress.
Conclusion: This study highlights the hepatoprotective effect of PN against H2O2-induced oxidative stress and the associated mechanisms.
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