|
|
|
|
Vol. 61, Issue 3, 554-561, March 2002
Department of Biochemistry (G.S., V.C., A.M.G.S.) and Department of
Experimental and Clinical Pharmacology (G.S.), Faculty of Medicine,
University of Catania, Catania, Italy; and Vascular Biology Unit,
Department of Surgical Research, Northwick Park Institute for Medical
Research, Harrow, Middlesex, United Kingdom (R.F., C.J.G., R.M.)
Heme oxygenase-1 (HO-1) is a redox-sensitive inducible protein that
provides efficient cytoprotection against oxidative stress. Curcumin, a
polyphenolic natural compound that possesses anti-tumor and
anti-inflammatory properties, has been reported recently to induce
potently HO-1 expression in vascular endothelial cells (Free Rad
Biol Med 28:1303-1312, 2000). Here, we extend our
previous findings by showing that caffeic acid phenethyl ester (CAPE),
another plant-derived phenolic agent, markedly increases heme oxygenase
activity and HO-1 protein in astrocytes. The effect seems to be related
to the peculiar chemical structures of curcumin and CAPE, because
analogous antioxidants containing only portions of these two molecules
were totally ineffective. At a final concentration of 30 µM, both
curcumin and CAPE maximally up-regulated heme oxygenase activity while
promoting marked cytotoxicity at higher concentrations (50-100 µM).
Similar results were obtained with Curcumin-95, a mixture of
curcuminoids commonly used as a dietary supplement. Incubation of
astrocytes with curcumin or CAPE at concentrations that promoted
maximal heme oxygenase activity resulted in an early increase in
reduced glutathione followed by a significant elevation in oxidized
glutathione contents. A curcumin-mediated increase in heme oxygenase
activity was not affected by the glutathione precursor and thiol donor
N-acetyl-L-cysteine. These data
suggest that regulation of HO-1 expression by polyphenolic compounds is evoked by a distinctive mechanism which is not necessarily linked to
changes in glutathione but might depend on redox signals sustained by
specific and targeted sulfydryl groups. This study identifies a novel
class of natural substances that could be used for therapeutic purposes
as potent inducers of HO-1 in the protection of tissues against
inflammatory and neurodegenerative conditions.
This article has been cited by other articles:
![]() |
C. I. Schwer, A. M. Guerrero, M. Humar, M. Roesslein, U. Goebel, P. Stoll, K. K. Geiger, B. H. J. Pannen, A. Hoetzel, and R. Schmidt Heme Oxygenase-1 Inhibits the Proliferation of Pancreatic Stellate Cells by Repression of the Extracellular Signal-Regulated Kinase1/2 Pathway J. Pharmacol. Exp. Ther., December 1, 2008; 327(3): 863 - 871. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Javvadi, A. T. Segan, S. W. Tuttle, and C. Koumenis The Chemopreventive Agent Curcumin Is a Potent Radiosensitizer of Human Cervical Tumor Cells via Increased Reactive Oxygen Species Production and Overactivation of the Mitogen-Activated Protein Kinase Pathway Mol. Pharmacol., May 1, 2008; 73(5): 1491 - 1501. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. G. Abraham and A. Kappas Pharmacological and Clinical Aspects of Heme Oxygenase Pharmacol. Rev., March 1, 2008; 60(1): 79 - 127. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Alam and J. L. Cook How Many Transcription Factors Does It Take to Turn On the Heme Oxygenase-1 Gene? Am. J. Respir. Cell Mol. Biol., February 1, 2007; 36(2): 166 - 174. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y.-S. Keum, S. Yu, P. P.-J. Chang, X. Yuan, J.-H. Kim, C. Xu, J. Han, A. Agarwal, and A.-N. T. Kong Mechanism of Action of Sulforaphane: Inhibition of p38 Mitogen-Activated Protein Kinase Isoforms Contributing to the Induction of Antioxidant Response Element-Mediated Heme Oxygenase-1 in Human Hepatoma HepG2 Cells. Cancer Res., September 1, 2006; 66(17): 8804 - 8813. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Erdmann, N. Grosser, K. Schipporeit, and H. Schroder The ACE Inhibitory Dipeptide Met-Tyr Diminishes Free Radical Formation in Human Endothelial Cells via Induction of Heme Oxygenase-1 and Ferritin J. Nutr., August 1, 2006; 136(8): 2148 - 2152. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. W. Ryter, J. Alam, and A. M. K. Choi Heme Oxygenase-1/Carbon Monoxide: From Basic Science to Therapeutic Applications Physiol Rev, April 1, 2006; 86(2): 583 - 650. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Abuarqoub, R. Foresti, C. J. Green, and R. Motterlini Heme oxygenase-1 mediates the anti-inflammatory actions of 2'-hydroxychalcone in RAW 264.7 murine macrophages Am J Physiol Cell Physiol, April 1, 2006; 290(4): C1092 - C1099. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. K. Andreadi, L. M. Howells, P. A. Atherfold, and M. M. Manson Involvement of Nrf2, p38, B-Raf, and Nuclear Factor-{kappa}B, but Not Phosphatidylinositol 3-Kinase, in Induction of Hemeoxygenase-1 by Dietary Polyphenols Mol. Pharmacol., March 1, 2006; 69(3): 1033 - 1040. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. D. Maines New Insights into Biliverdin Reductase Functions: Linking Heme Metabolism to Cell Signaling Physiology, December 1, 2005; 20(6): 382 - 389. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Wu and R. Wang Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications Pharmacol. Rev., December 1, 2005; 57(4): 585 - 630. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. M. Ogborne, S. A. Rushworth, and M. A. O'Connell {alpha}-Lipoic Acid-Induced Heme Oxygenase-1 Expression Is Mediated by Nuclear Factor Erythroid 2-Related Factor 2 and p38 Mitogen-Activated Protein Kinase in Human Monocytic Cells Arterioscler. Thromb. Vasc. Biol., October 1, 2005; 25(10): 2100 - 2105. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Wijayanti, T. Kietzmann, and S. Immenschuh Heme Oxygenase-1 Gene Activation by the NAD(P)H Oxidase Inhibitor 4-(2-Aminoethyl) Benzenesulfonyl Fluoride via a Protein Kinase B, p38-dependent Signaling Pathway in Monocytes J. Biol. Chem., June 10, 2005; 280(23): 21820 - 21829. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Foresti, M. Hoque, D. Monti, C. J. Green, and R. Motterlini Differential Activation of Heme Oxygenase-1 by Chalcones and Rosolic Acid in Endothelial Cells J. Pharmacol. Exp. Ther., February 1, 2005; 312(2): 686 - 693. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. F. Poon, V. Calabrese, G. Scapagnini, and D. A. Butterfield Free Radicals: Key to Brain Aging and Heme Oxygenase as a Cellular Response to Oxidative Stress J. Gerontol. A Biol. Sci. Med. Sci., May 1, 2004; 59(5): M478 - M493. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Martin, A. I. Rojo, M. Salinas, R. Diaz, G. Gallardo, J. Alam, C. M. R. de Galarreta, and A. Cuadrado Regulation of Heme Oxygenase-1 Expression through the Phosphatidylinositol 3-Kinase/Akt Pathway and the Nrf2 Transcription Factor in Response to the Antioxidant Phytochemical Carnosol J. Biol. Chem., March 5, 2004; 279(10): 8919 - 8929. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Colombrita, V. Calabrese, A. M. G. Stella, F. Mattei, D. L. Alkon, and G. Scapagnini Regional Rat Brain Distribution of Heme Oxygenase-1 and Manganese Superoxide Dismutase mRNA: Relevance of Redox Homeostasis in the Aging Processes Experimental Biology and Medicine, May 1, 2003; 228(5): 517 - 524. [Abstract] [Full Text] [PDF] |
||||