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http://dx.doi.org/10.4162/nrp.2014.8.1.125

Black rice extract protected HepG2 cells from oxidative stress-induced cell death via ERK1/2 and Akt activation  

Yoon, Jaemin (Department of Food Science and Technology, Chungbuk National University)
Ham, Hyeonmi (Department of Food Science and Technology, Chungbuk National University)
Sung, Jeehye (Department of Food Science and Technology, Chungbuk National University)
Kim, Younghwa (Department of Food Science and Technology, Chungbuk National University)
Choi, Youngmin (National Academy of Agricultural Science, Rural Development Administration)
Lee, Jeom-Sig (National Institute of Crop Science, Rural Development Administration)
Jeong, Heon-Sang (Department of Food Science and Technology, Chungbuk National University)
Lee, Junsoo (Department of Food Science and Technology, Chungbuk National University)
Kim, Daeil (Department of Horticultural Science, Chungbuk National University)
Publication Information
Nutrition Research and Practice / v.8, no.2, 2014 , pp. 125-131 More about this Journal
Abstract
BACKGROUND/OBJECTIVES: The objective of this study was to evaluate the protective effect of black rice extract (BRE) on tert-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 oxidative injury in HepG2 cells. Several biomarkers that modulate cell survival and death including reactive oxygen species (ROS), caspase-3 activity, 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 generation and also by preventing ERKs deactivation and the prolonged JNKs activation. Moreover, pretreatment of BRE increased the activation of ERKs and Akt which are pro-survival signal proteins. However, this effect was blunted in the presence of ERKs and Akt inhibitors. CONCLUSIONS: These results suggest that activation of ERKs and Akt pathway might be involved in the cytoprotective effect of BRE against oxidative stress. Our findings provide new insights into the cytoprotective effects and its possible mechanism of black rice against oxidative stress.
Keywords
Black rice; HepG2; oxidative stress; ERK1/2; Akt;
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