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1 Division of Nephrology, Hypertension and Transplantation, Department of Medicine, 2 Department of Neuroscience, and 3 Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida 32610
First published August 9, 2001;
10.1152/ajprenal.00140.2001.
Heme oxygenase-1 (HO-1) catalyzes
the rate-limiting step in heme degradation, releasing iron, carbon
monoxide, and biliverdin. Induction of HO-1 occurs as an adaptive and
protective response to several inflammatory stimuli. The transcription
factor activator protein-1 (AP-1) has been implicated in the activation
of the HO-1 gene. To elucidate the molecular mechanism of HO-1
induction, we examined the effects of diferuloylmethane (curcumin), an
inhibitor of the transcription factor AP-1. Surprisingly, curcumin by
itself was a very potent inducer of HO-1. Curcumin has
anti-inflammatory, antioxidant, and renoprotective effects. To evaluate
the mechanism of curcumin-mediated induction of HO-1, confluent human
renal proximal tubule cells were exposed to curcumin (1-8 µM).
We observed a time- and dose-dependent induction of HO-1 mRNA that was
associated with increased HO-1 protein. Coincubation of curcumin with
actinomycin D completely blocked the upregulation of HO-1 mRNA.
Blockade of nuclear factor-
B (NF-B) with an IB
phosphorylation inhibitor attenuated curcumin-mediated induction of
HO-1 mRNA and protein. These data demonstrate that curcumin induces
HO-1 mRNA and protein in renal proximal tubule cells. HO-1 induction by
curcumin is mediated, at least in part, via transcriptional mechanisms
and involves the NF-B pathway.
antioxidants; nuclear factor-B; renal tubular injury
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