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Involvement of ERK, Akt and JNK signalling in H 2 O 2 ‐induced cell injury and protection by hydroxytyrosol and its metabolite homovanillic alcohol
Author(s) -
Incani Alessandra,
Deiana Monica,
Corona Giulia,
Vafeiadou Katerina,
Vauzour David,
Dessì M. Assunta,
Spencer Jeremy P. E.
Publication year - 2010
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200900098
Subject(s) - hydroxytyrosol , protein kinase b , chemistry , metabolite , mapk/erk pathway , oxidative stress , hydrogen peroxide , kinase , homovanillic acid , pi3k/akt/mtor pathway , oxidative phosphorylation , kidney , biochemistry , pharmacology , programmed cell death , phosphorylation , signal transduction , apoptosis , polyphenol , biology , endocrinology , antioxidant , receptor , serotonin
The olive oil polyphenol, hydroxytyrosol (HT), is believed to be capable of exerting protection against oxidative kidney injury. In this study we have investigated the ability of HT and its O ‐methylated metabolite, homovanillic alcohol (HVA) to protect renal cells against oxidative damage induced by hydrogen peroxide. We show that both compounds were capable of inhibiting hydrogen peroxide‐induced kidney cell injury via an ability to interact with both MAP kinase and PI3 kinase signalling pathways, albeit at different concentrations. HT strongly inhibited death and prevented peroxide‐induced increases in ERK1/2 and JNK1/2/3 phosphorylation at 0.3 μM, whilst HVA was effective at 10 μM. At similar concentrations, both compounds also prevented peroxide‐induced reductions in Akt phosphorylation. We suggest that one potential protective effect exerted by olive oil polyphenols against oxidative kidney cell injury may be attributed to the interactions of HT and HVA with these important intracellular signalling pathways.