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The Ethanol Precipitate of U lva rigida Protects HeLa Cells from Hydrogen Peroxide‐Induced Apoptosis
Author(s) -
Mezghani Sana,
N'Guessan Prudence,
Carrier Alice,
Amri Mohamed
Publication year - 2015
Publication title -
journal of food biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.507
H-Index - 47
eISSN - 1745-4514
pISSN - 0145-8884
DOI - 10.1111/jfbc.12106
Subject(s) - hela , apoptosis , oxidative stress , hydrogen peroxide , antioxidant , downregulation and upregulation , chemistry , microbiology and biotechnology , cell , biochemistry , biology , gene
AbstractU lva rigida exhibits antioxidant activity that protects against oxidative stress. In the present investigation, we conducted experiments in HeLa cells exposed to hydrogen peroxide ( H 2 O 2 ) and found that the U . rigida ethanolic precipitate inhibited H 2 O 2 apoptosis. This precipitate prevented the H 2 O 2 stress‐induced decline in the mitochondrial membrane potential ( MMP ). P21 Bax expression was decreased in H 2 O 2 ‐treated cells compared with untreated cells. Conversely, p21 Bax was consistently detected in cells that were co‐treated with H 2 O 2 and the U . rigida ethanolic precipitate. Bcl ‐ xL expression increased in cells co‐treated with H 2 O 2 and the U . rigida ethanolic precipitate compared with H 2 O 2 ‐treated cells. Based on the obtained results, H 2 O 2 ‐induced apoptosis was inhibited by the U . rigida ethanol precipitate early in the apoptotic process through the upregulation of Bcl ‐ xL , the prevention of full‐length Bax cleavage molecule and the subsequent inhibition of MMP loss, which is a crucial step in the apoptotic cascade. Practical Applications Increasing evidence from both experimental and clinical studies has suggested that oxidative stress plays a major role in aging and pathogenesis. Currently, the search for safe and efficacious medicinal plants that possess antioxidant activity has attracted particular interest. In this context, this is the first report on the antioxidant activity of U lva rigida in a cell line: U . rigida protected the cells from oxidative stress‐induced apoptosis. The U . rigida ethanol precipitate inhibited apoptosis via the upregulation of Bcl ‐ xL , the prevention of full‐length Bax cleavage to its short and potent form, and the subsequent inhibition of the loss of the mitochondrial membrane potential. Herein, we report the mechanism by which U . rigida protects against oxidative stress‐induced apoptosis. This may provide knowledge to enable the development of novel therapeutic strategies using U . rigida compounds to treat diseases that are attributed to oxidative disorders.