Curcumin and the Heart
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Curcumin may cut heart failure risk says research duo
By Stephen Daniells; 25-Feb-2008 –
Curcumin, the natural pigment that gives the spice turmeric its yellow colour, may protect against heart failure - in mice
at least - suggests a new study from Canada.
When the pigment was given to mice with enlarged hearts (hypertrophy), heart function was restored and scar
formation reduced, report the researchers in the February edition of the Journal of Clinical Investigation. Lead
researcher Peter Liu, scientific director at the Canadian Institutes of Health Research - Institute of Circulatory and
Respiratory Health said that curcumin might be a safe and effective means of preventing heart failure in the future,
given that it is naturally occurring and readily available at a low cost.
"Whether you are young or old; male or female; the larger your heart is, the higher your risk is for developing heart
attacks or heart failure in the future. However, until clinical trials are done, we don't recommend patients to take
curcumin routinely. You are better off to take action today by lowering blood pressure, reducing cholesterol,
exercising and healthy eating," he said.
Curcumin has come under the scientific spotlight in recent years, with studies investigating its potential benefits for
reducing cholesterol levels, improving cardiovascular health, and fighting cancer.
Some experts recommend however that consumers wishing to make use of curcumin's properties consume it in
supplement form rather than eating more curries, which tend to be rather high in fat in their Western form.
The Canadian researchers found that curcumin appeared to work by preventing abnormal unravelling of the
chromosome under stress, in addition to preventing excessive abnormal protein production. The pigment was
administered as a curcumin suspension using 0.5 per cent carboxy-methylcellulose solution,
"Curcumin's ability to shut off one of the major switches right at the chromosome source where the enlargement and
scarring genes are being turned on is impressive," said Liu. However he cautioned that moderation is important, "the
beneficial effects of curcumin are not strengthened by eating more of it."
Specifically, the pigment was found to act on p300-histone acetyltransferase (HAT), reportedly the most important HAT
in muscle that "modifies chromatin and associated transcription factors and promotes gene activation," wrote the
researchers.
The study was funded by the Heart and Stroke Foundation and the Canadian Institutes of Health Research.
"This study is relevant to the understanding of the inhibitory effect of curcumin on cardiac hypertrophy and related
molecular mechanisms," wrote the researchers. "It also serves to elucidate the dominant signaling pathways leading to
cardiac hypertrophy, inflammation, and fibrosis in response to hypertrophic stimuli."
"Curcumin is a natural polyphenolic compound that has already been used clinically and is approved by the FDA as a
safe food additive. Future studies should examine the hypothesis that curcumin may be a safe and effective approach
to preventing and treating cardiac hypertrophy and the transition to failure," they concluded.
Supporting data
In a related article in the same journal, Tatsuya Morimoto and co-workers from the National Hospital Organization in
Kyoto report similar findings from a study with rats. The Japanese researchers tested curcumin in two models of heart
failure - heart disease associated with high blood pressure in salt-sensitive rats, and surgically-induced myocardial
infarction in rats.
They report that, in both cases, the pigment prevented increases in heart muscle wall thickness after heart failure.
"We believe that the use of curcumin, which targets nuclear signaling pathways in cardiomyocytes, will provide a novel
therapeutic strategy against heart failure," wrote Morimoto and co-workers. "Future application of this nontoxic dietary
natural compound as a therapeutic agent for heart failure in humans would be particularly interesting."
Curcumin-based treatments are currently in clinical trials for pancreatic and colorectal cancer patients with promising
results.
Sources: Journal of Clinical Investigation
Available online, Free Access, doi: 10.1172/JCI32865
"Curcumin prevents and reverses murine cardiac hypertrophy"
Authors: Hong-Liang Li, C. Liu, G. de Couto, M. Ouzounian, M. Sun, A.-B. Wang, Y. Huang, C.-W. He, Y. Shi, X. Chen, M.P.
Nghiem, Y. Liu, M. Chen, F. Dawood, M. Fukuoka, Y. Maekawa, L. Zhang, A. Leask, A.K. Ghosh, L.A. Kirshenbaum, P.P. Liu
Journal of Clinical Investigation
Available online, Free Access, doi: 10.1172/JCI33160
J Clin Invest. 2008 Feb 21 [Epub ahead of print]Links
Curcumin prevents and reverses murine cardiac hypertrophy.
Li HL, Liu C, de Couto G, Ouzounian M, Sun M, Wang AB, Huang Y, He CW, Shi Y, Chen X, Nghiem MP, Liu Y, Chen M,
Dawood F, Fukuoka M, Maekawa Y, Zhang L, Leask A, Ghosh AK, Kirshenbaum LA, Liu PP.
Division of Cardiology, Heart and Stroke/Richard Lewar Centre of Excellence, University Health Network, University
of Toronto, Toronto, Ontario, Canada. Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, NIH,
Bethesda, Maryland, USA. Wellcome Trust Genome Campus and Sanger Institute, Hinxton, Cambridge, United Kingdom.
Department of Medicine, Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Division of Oral Biology and Department of Physiology and Pharmacology, Canadian Institutes of Health Research
(CIHR) Group in Skeletal Development and Remodeling, Schulich School of Medicine and Dentistry, University of
Western Ontario, London, Ontario, Canada. Division of Rheumatology, Northwestern University Feinberg School of
Medicine, Chicago, Illinois, USA. Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre,
Winnipeg, Manitoba, Canada. Institute of Circulatory and Respiratory Health, Canadian Institutes of Health Research,
Ottawa, Ontario, Canada.
Chromatin remodeling, particularly histone acetylation, plays a critical role in the progression of pathological cardiac
hypertrophy and heart failure. We hypothesized that curcumin, a natural polyphenolic compound abundant in the spice
turmeric and a known suppressor of histone acetylation, would suppress cardiac hypertrophy through the disruption of
p300 histone acetyltransferase-dependent (p300-HAT-dependent) transcriptional activation. We tested this hypothesis
using primary cultured rat cardiac myocytes and fibroblasts as well as two well-established mouse models of cardiac
hypertrophy. Curcumin blocked phenylephrin-induced (PE-induced) cardiac hypertrophy in vitro in a dose-dependent
manner. Furthermore, curcumin both prevented and reversed mouse cardiac hypertrophy induced by aortic banding
(AB) and PE infusion, as assessed by heart weight/BW and lung weight/BW ratios, echocardiographic parameters, and
gene expression of hypertrophic markers. Further investigation demonstrated that curcumin abrogated histone
acetylation, GATA4 acetylation, and DNA-binding activity through blocking p300-HAT activity. Curcumin also blocked AB-
induced inflammation and fibrosis through disrupting p300-HAT-dependent signaling pathways. Our results indicate
that curcumin has the potential to protect against cardiac hypertrophy, inflammation, and fibrosis through suppression
of p300-HAT activity and downstream GATA4, NF-kappaB, and TGF-beta-Smad signaling pathways.
J Clin Invest. 2008 Feb 21 [Epub ahead of print]Links
Currying favor for the heart.
Epstein JA.
Department of Cell and Developmental Biology, Cardiovascular Institute, and Institute for Regenerative Medicine,
University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Curcumin, a commonly available spice and alternative medicine, has been tested in the laboratory and the clinic for
activity against a wide range of diseases. It is thought to possess antiinflammatory and antioxidant activities and may
also function to inhibit histone acetyl transferases, which activate gene expression via chromatin remodeling. Two
reports in this issue of the JCI, by Morimoto et al. and Li et al., suggest that curcumin may inhibit cardiac hypertrophy in
rodent models and provide beneficial effects after myocardial infarction or in the setting of hypertension (see the
related articles, doi:10.1172/JCI33160 and 10.1172/JCI32865, respectively). These results will spur further mechanistic
inquiry into the role of chromatin remodeling in the regulation of cardiac homeostasis.
J Clin Invest. 2008 Feb 21 [Epub ahead of print]Links
The dietary compound curcumin inhibits p300 histone acetyltransferase activity and prevents heart failure in rats.
Morimoto T, Sunagawa Y, Kawamura T, Takaya T, Wada H, Nagasawa A, Komeda M, Fujita M, Shimatsu A, Kita T,
Hasegawa K.
Division of Translational Research, Kyoto Medical Center, National Hospital Organization, Kyoto, Japan. Department
of Cardiovascular Medicine, Department of Cardiovascular Surgery, and Department of Human Health Sciences,
Graduate School of Medicine, Kyoto University, Kyoto, Japan. Clinical Research Institute, Kyoto Medical Center,
National Hospital Organization, Kyoto, Japan.
Hemodynamic overload in the heart can trigger maladaptive hypertrophy of cardiomyocytes. A key signaling event in
this process is nuclear acetylation by histone deacetylases and p300, an intrinsic histone acetyltransferase (HAT). It has
been previously shown that curcumin, a polyphenol responsible for the yellow color of the spice turmeric, possesses
HAT inhibitory activity with specificity for the p300/CREB-binding protein. We found that curcumin inhibited the
hypertrophy-induced acetylation and DNA-binding abilities of GATA4, a hypertrophy-responsive transcription factor, in
rat cardiomyocytes. Curcumin also disrupted the p300/GATA4 complex and repressed agonist- and p300-induced
hypertrophic responses in these cells. Both the acetylated form of GATA4 and the relative levels of the p300/GATA4
complex markedly increased in rat hypertensive hearts in vivo. The effects of curcumin were examined in vivo in 2
different heart failure models: hypertensive heart disease in salt-sensitive Dahl rats and surgically induced myocardial
infarction in rats. In both models, curcumin prevented deterioration of systolic function and heart failure-induced
increases in both myocardial wall thickness and diameter. From these results, we conclude that inhibition of p300 HAT
activity by the nontoxic dietary compound curcumin may provide a novel therapeutic strategy for heart failure in
humans.
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