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Methyl gallate attenuate cadmium‐induced cytotoxicity by heme oxygenase‐1 in cultured mouse mesangial cells
Author(s) -
Cha Seok Ho,
Lee Woon Kyu,
Suh Chang Kook
Publication year - 2009
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.23.1_supplement.604.7
Subject(s) - heme oxygenase , propyl gallate , methyl gallate , viability assay , chemistry , cytotoxicity , zinc protoporphyrin , microbiology and biotechnology , gallate , messenger rna , biochemistry , heme , biology , cell , antioxidant , in vitro , enzyme , nuclear chemistry , gallic acid , gene
The purpose of this study is to investigate the protective effect of methyl gallate (MG), a phytochemical, on cadmium (Cd)‐induced renal toxicity related by heme oxygenase‐1 (HO‐1) expression using cultured mouse mesangial cell line (MMC). By employing RT‐PCR and Western blotting techniques, we have examined the HO‐1 induction in MMCs that were treated with Cd or Methyl gallate. By employing a cell viability assay, we have also examined the cytoprotective effect of HO‐1 induction against the cytotoxicity caused by toxic dose of Cd. In MMCs exposed to Cd and methyl gallate, expression of HO‐1 (mRNA and protein) was increased in a dose‐ and time‐dependent manner. The up‐regulation of HO‐1 mRNA and protein expressions by Cd and methyl gallate was inhibited by a pre‐incubation of the cells with actinomycin D, an inhibitor of mRNA transcription. Upon the inhibition of elevated HO‐1 mRNA and protein expressions by the use of zinc protoporphyrin IX (ZnPP), an inhibitor of HO‐1 activity, the change of HO‐1 mRNA and protein expressions by ZnPP was not observed. The decreased viability of the cells by Cd was partially recovered by the treatment with methyl gallate. These cytotoxic and cytoprotective effect was dramatically decreased by the treatment with ZnPP. From these results, methyl gallate have cytoprotective effect that related with heme oxygenase‐1 activity.