Antioxidative mechanisms of sea buckthorn fruit extract in mouse embryonic fibroblast cells

This study was conducted to define the antioxidant properties and cytoprotective mechanisms of sea buckthorn fruit extract (SFE) against cellular oxidative stress in mouse embryonic fibroblast (MEF) cells. Cell viability of MEF cells damaged by H 2 O 2 was significantly increased by addition of SFE...

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Published inFood science and biotechnology Vol. 22; no. Suppl 1; pp. 197 - 204
Main Authors Lim, Sae-Rom, Go, Eun-Bi, Go, Geon, Shin, Han-Seung, Sung, Jung-Suk
Format Journal Article
LanguageEnglish
Published Heidelberg The Korean Society of Food Science and Technology 01.02.2013
한국식품과학회
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Summary:This study was conducted to define the antioxidant properties and cytoprotective mechanisms of sea buckthorn fruit extract (SFE) against cellular oxidative stress in mouse embryonic fibroblast (MEF) cells. Cell viability of MEF cells damaged by H 2 O 2 was significantly increased by addition of SFE in a concentration dependent manner. Cytoprotective effect of SFE against oxidative damage was observed to be co-related with regulation of cell cycle progression. Induction of cell cycle arrest in G 2 / M checkpoint was mediated by oxidative stress, but significantly reduced by treatment of MEF cells with SFE. Analysis of key regulatory proteins involved in G 2 /M arrest showed that SFE treatment leads to down-regulation of both phosphorylated Chk1 and cyclin B, which play important roles in cell cycle arrest of oxidatively damaged cells. Effect of SFE on apoptosis was evaluated by morphological and flow cytometric analysis. Apoptotic cell accumulation occurred by H 2 O 2 treatment was decreased by co-treatment of MEF cells with SFE. Early apoptotic process involved in DNA fragmentation and condensation was also inhibited by additional treatment with SFE. Overall results suggest that cytoprotective effect of SFE is mediated by effective radical scavenging activity as well as altered cell cycle regulation which prevent apoptotic cell death induced by cellular oxidative stress.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
G704-000139.2013.22..020
ISSN:1226-7708
2092-6456
DOI:10.1007/s10068-013-0067-z