Black rice extract protected HepG2 cells from oxidative stress-induced cell death via ERK1/2 and Akt activation
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BACKGROUND/OBJECTIVES: The objective of this study was to evaluate the protective effect of black rice extract (BRE) ontert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells. MATERIALS/METHODS: Methanolic extract from black rice was evaluated for the protective effect on TBHP-induced oxidativeinjury in HepG2 cells. Several biomarkers that modulate cell survival and death including reactive oxygen species (ROS), caspase-3activity, and related cellular kinases were determined. RESULTS: TBHP induced cell death and apoptosis by a rapid increase in ROS generation and caspase-3 activity. Moreover,TBHP-induced oxidative stress resulted in a transient ERK1/2 activation and a sustained increase of JNK1/2 activation. While,BRE pretreatment protects the cells against oxidative stress by reducing cell death, caspase-3 activity, and ROS generationand also by preventing ERKs deactivation and the prolonged JNKs activation. Moreover, pretreatment of BRE increased theactivation of ERKs and Akt which are pro-survival signal proteins. However, this effect was blunted in the presence of ERKsand Akt inhibitors. CONCLUSIONS: These results suggest that activation of ERKs and Akt pathway might be involved in the cytoprotective effectof BRE against oxidative stress. Our findings provide new insights into the cytoprotective effects and its possible mechanismof black rice against oxidative stress.
Abstract
BACKGROUND/OBJECTIVES: The objective of this study was to evaluate the protective effect of black rice extract (BRE) ontert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells. MATERIALS/METHODS: Methanolic extract from black rice was evaluated for the protective effect on TBHP-induced oxidativeinjury in HepG2 cells. Several biomarkers that modulate cell survival and death including reactive oxygen species (ROS), caspase-3activity, and related cellular kinases were determined. RESULTS: TBHP induced cell death and apoptosis by a rapid increase in ROS generation and caspase-3 activity. Moreover,TBHP-induced oxidative stress resulted in a transient ERK1/2 activation and a sustained increase of JNK1/2 activation. While,BRE pretreatment protects the cells against oxidative stress by reducing cell death, caspase-3 activity, and ROS generationand also by preventing ERKs deactivation and the prolonged JNKs activation. Moreover, pretreatment of BRE increased theactivation of ERKs and Akt which are pro-survival signal proteins. However, this effect was blunted in the presence of ERKsand Akt inhibitors. CONCLUSIONS: These results suggest that activation of ERKs and Akt pathway might be involved in the cytoprotective effectof BRE against oxidative stress. Our findings provide new insights into the cytoprotective effects and its possible mechanismof black rice against oxidative stress.
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