Turmeric (Curcumin)
Turmeric is an anti-inflammatory and antioxidant herb useful for haemorrhage, and with major active constituents being curcuminoids, including curcumin (diferuloylmethane), it has good anti-inflammatory activity, possibly by inhibiting cyclooxygenase-2 (COX-2), prostaglandins and leukotrienes. Curcumin may have antithrombotic effects. Other research suggests that turmeric might have lipid lowering and immunostimulatory effects. It also seems to have activity against some bacteria.
May be beneficial in atherosclerosis, as well as many other anti-inflammatory uses.
Research indicates that the curcumin compound in turmeric is good for not only preventing heart failure but also repairing damage that's already happened. Curcumin may turn off genes that enlarge the heart and cause scarring.
Clinical Studies
Turmeric
Turmeric Component Curcumin Improves Cardiovascular Function
Curcumin, the yellow pigment found in turmeric, prevented heart failure in animals in two recently released studies.
In the first study, curcumin appeared to reduce cardiac hypertrophy, the enlargement of the heart. The larger an individual’s heart, the higher his or her risk for developing heart attacks or heart failure.
Histone acetylation plays a critical role in the progression of pathological cardiac hypertrophy and heart failure. Consequently, researchers hypothesized that curcumin, a known suppressor of histone acetylation, would suppress cardiac hypertrophy. They tested this hypothesis in vitro using cultured cells from rats’ heart muscle as well as in vivo during two well-established mouse models of cardiac hypertrophy. The result indicated that curcumin blocked cardiac hypertrophy in vitro in a dose-dependent manner. Furthermore, curcumin both prevented and reversed mouse cardiac hypertrophy. Further investigation demonstrated that curcumin did indeed suppress histone acetylation. Curcumin also blocked inflammation and fibrosis.
In the second study, researchers came to a similar conclusion. In this study, curcumin’s effects were examined in vivo in 2 different heart failure models: hypertensive heart disease in salt-sensitive rats and surgically induced myocardial infarction in rats. In both models, curcumin prevented deterioration of systolic function and prevented heart failure–induced increases in both myocardial wall thickness and diameter.
According to the researchers, “…the nontoxic dietary compound curcumin may provide a novel therapeutic strategy for heart failure in humans.”
Journal of Clinical Investigation. February 21, 2008
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.
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.
PMID: 18292809 [PubMed - indexed for MEDLINE]
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.
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.
PMID: 18292803 [PubMed - indexed for MEDLINE]
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.
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.
PMID: 18292803 [PubMed - indexed for MEDLINE]
Mechanism of the Anti-inflammatory Effect of Curcumin: PPAR-gamma Activation
Jacob A, Wu R, Zhou M, Wang P.
Division of Surgical Research, North Shore University Hospital and Long Island Jewish Medical Center, 350 Community Drive, Manhasset, NY 11030, USA.
Curcumin, the phytochemical component in turmeric, is used as a dietary spice and a topical ointment for the treatment of inflammation in India for centuries. Curcumin (diferuloylmethane) is relatively insoluble in water, but dissolves in acetone, dimethylsulphoxide, and ethanol. Commercial grade curcumin contains 10-20% curcuminoids, desmethoxycurcumin, and bisdesmethoxycurcumin and they are as effective as pure curcumin. Based on a number of clinical studies in carcinogenesis, a daily oral dose of 3.6 g curcumin has been efficacious for colorectal cancer and advocates its advancement into Phase II clinical studies. In addition to the anticancer effects, curcumin has been effective against a variety of disease conditions in both in vitro and in vivo preclinical studies. The present review highlights the importance of curcumin as an anti-inflammatory agent and suggests that the beneficial effect of curcumin is mediated by the upregulation of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation.
PMID: 18274631 [PubMed - in process]