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Dietary iodole 3, 3′‐diindolylmethane protects cultured human alveolar epithelial cells from oxidative stress induced cell death
Author(s) -
galam lakshmi,
Prasanna TP,
younus Asfiya,
Hodgkins Amanda,
Gurukumar KR,
Cox Ruan R,
Jutaro F,
Lockey Richard F,
Kolliputi Narasaiah
Publication year - 2012
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.26.1_supplement.lb684
Subject(s) - oxidative stress , programmed cell death , apoptosis , a549 cell , microbiology and biotechnology , chemistry , necrosis , cell growth , cell , cancer research , biology , medicine , biochemistry , pathology
Dietary indoles including indole‐3‐carbinol (I3C) and its derivative, diindolylmethane (DIM) are found in cruciferous vegetables have been known for their anti cancer and anti‐inflammatory properties. Oxidative stress and alveolar epithelial cell death play a key role in the pathogenesis of several pulmonary diseases. In this report, we investigated the protective ability of DIM to ameliorate oxidative stress and alveolar epithelial cell death in vitro . Human type II alveolar epithelial cells (A549) were treated with the oxidative stress inducer hydrogen peroxide (H 2 O 2 ), in the presence and absence of DIM. In another set of experiments, we first induced apoptosis by starvation in epithelial cells and then post treated with DIM to determine the reversal of epithelial cell apoptosis. The results showed that the compound DIM inhibited the H 2 O 2 induced the alveolar epithelial cell necrosis and apoptosis. This property of DIM ensured the protection of alveolar epithelial cells from oxidative stress induced cell death. In addition DIM also reverses cell death and protects alveolar epithelial cells from starvation induced cell damage and cell death. Taken together our data demonstrated that the natural dietary compound DIM attenuates oxidative stress induced epithelial cell death. This work is supported by R01 HL105932 (NIH) and AmericanHeart Association National Scientist Development Grant 09SDG2260957