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Akebiae caulis extract inhibits oxidative stress through AMPK/GSK3‐beta pathway (LB551)
Author(s) -
Kim Young Woo,
Jung Eun Hye,
Byun Sung Hui,
Kim Sang Chan,
Cho Il Je
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb551
Subject(s) - ampk , cytoprotection , oxidative stress , chemistry , mitochondrion , phosphorylation , reactive oxygen species , microbiology and biotechnology , amp activated protein kinase , pharmacology , protein kinase a , biochemistry , medicine , biology
Akebiae caulis is commonly used for the oposiuria, inflammation, nociceptive and fever. We investigated the effect of Akebiae Caulis extract (ACE) to protect cells against the mitochondrial dysfunction and apoptosis. Arachidonic acid (AA)+iron promotes excessive reactive oxygen species production and dysfunction of mitochondria. ACE protected hepatocytes from AA+iron‐induced cytotoxicity. As a potential molecular mechanism for the ACE‐mediated cytoprotection, phosphorylation of AMPK, a key regulator in determining cell survival or death, was increased by ACE. Moreover, ACE treatment enhanced inactive phosphorylation of GSK3β, downstream substrate kinase of AMPK. ACE also prevented a decrease in the GSK3β phosphorylation derived by AA+iron, which might contribute to mitochondrial protection and cell survival. Moreover, we found that betulin in combination with hederagenin protected from AA+iron‐induced mitochondrial dysfunction. These results show that ACE has the ability to protect cells against AA+iron‐induced H 2 O 2 production and mitochondrial impairment, which is mediated with inactive GSK3β phosphorylation downstream of AMPK. Grant Funding Source : This work was supported by the National Research Foundation of Korea grant funded by the Korea government [MEST](No.2012‐0009400).