Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets

Srivastava, K. C.; Bordia, A; Verma, Surendra Kumar

doi:10.1016/0952-3278(95)90040-3

Cited by 181 publications

(117 citation statements)

References 14 publications

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“…Previous intervention studies have shown that distinctive components of MD reduce platelet function, and this effect has been proposed as a mechanism contributing to the CV benefit of this diet. In fact, fish oils (Goodnight et al, 1981;Agren et al, 1997;Vognild et al, 1998), a-linolenic acid (Renaud & Nordøy, 1983;Allman et al, 1995;Freese et al, 1994) and various spices (Janssen et al, 1998;Ackerman et al, 2001;Srivastava et al, 1995) induce a decrease of platelet function. The apparent discrepancy of our results with those findings is probably explained by the lower content of each one of these substances in the complete MD, as opposed to the amounts used for single components of MD in selective intervention studies.…”

Section: Discussionmentioning

confidence: 99%

“…In this context, some of the beneficial effects of MD and wine consumption could be mediated by a reduction in platelet reactivity. Several studies report that diets enriched with fish, a-linolenic acid and spices, abundant in the case of MD, include substances that reduce or could reduce platelet function (Vognild et al, 1998;Allman et al, 1995;Janssen et al, 1998;Ackerman et al, 2001;Srivastava et al, 1995). Similarly, other reports indicate that the intake of moderate amounts of ethanol or nonalcoholic components of wine, for 2 or more weeks, is associated with a decrease in ex vivo platelet function (Pikkar et al, 1987;Pellegrini et al, 1996;Pace-Asciak et al, 1996;Freedman et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Mediterranean diet, but not red wine, is associated with beneficial changes in primary haemostasis

et al. 2003

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Objective: (1) To compare the effect of an alcohol-free Mediterranean-type diet (MD) and a high-fat diet (HFD) on variables of primary haemostasis (bleeding time, plasma von Willebrand factor and platelet aggregation=secretion). (2) To test whether red wine supplementation modified these variables, independently of the diet. Design, subjects and intervention: Controlled prospective intervention study. Two groups, each consisting of 21 healthy male university students (22 AE 3.4 y), received either MD or HFD during 90 days. Between days 30 and 60, both diets were supplemented with 240 ml=day of red wine. Baseline (T0) and T30, T60 and T90-day samples were drawn. Bleeding time was measured before (day 30) and after (day 60) wine supplementation. No drop out from the study was experienced. Setting: University campus and outpatient nutrition clinic. Results: All baseline (day 0) variables did not differ significantly between study groups. On day 30, individuals on MD had significantly higher levels of plasma b-carotene, folate, ascorbate, and eicosapentaenoic acid in plasma lipid fractions, than those on HFD. Total plasma cholesterol, HDL and LDL did not change significantly in either study group at any time point. After 30 days on each diet, individuals on MD had longer bleeding time (BT) than those on HFD (7.6 AE 2.8 vs 5.8 AE 1.7 min; P ¼ 0.017). BT did not change significantly after I month of wine supplementation (7.1 AE 2.0 vs 5.5 AE 2.0 min, respectively). Plasma von Willebrand factor (vWF : Ag) on day 0 was 89 AE 40 and 111 AE 70% in MD and HFD groups, respectively (P ¼ 0.21). These values did not change significantly at 30, 60 or 90 days. MD intake was associated with an increase in platelet serotonin secretion (P ¼ 0.02) and a marginal increase in platelet aggregation after stimulation with epinephrine (P ¼ 0.07). Wine intake resulted in a marginal decrease in platelet 14 C-5-HT secretion with 4 mM ADP (P ¼ 0.07). However, both platelet aggregation and secretion were consistently increased when using collagen as agonist (1 and 2 mg=ml, P ¼ 0.01). Conclusion: The longer BT in individuals on MD, obtained independently of red wine, denotes less interaction of platelets with the vascular wall, which could be beneficial from the point of view of cardiovascular (CV) risk. This effect is not explained by changes in the measured haemostatic determinants of BT (plasma vWF, ex vivo platelet function), and might be attributed to other as yet unknown vascular factors. Moderate consumption of red wine results in a significant increase in ex vivo platelet aggregation and secretion after stimulation with collagen. This observation contradicts previous reports, although further studies are required to elucidate the influence of this finding on CV risk.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mediterranean diet, but not red wine, is associated with beneficial changes in primary haemostasis

et al. 2003

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“…On the other hand, effects on COX isoenzymes might contribute to the general suppression of cellular prostanoid biosynthesis observed at higher curcumin concentrations (≥10 μmol/L; refs. 21,28,34). Along these lines, curcumin at 30 μmol/L Figure 3.…”

Section: Discussionmentioning

confidence: 99%

Curcumin blocks prostaglandin E2 biosynthesis through direct inhibition of the microsomal prostaglandin E2 synthase-1

Koeberle

Northoff

Werz

2009

Molecular Cancer Therapeutics

104

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Prostaglandin E 2 (PGE 2 ) plays a crucial role in the apparent link between tumor growth and chronic inflammation. Cyclooxygenase (COX)-2 and microsomal PGE 2 synthase-1, which are overexpressed in many cancers, are functionally coupled and thus produce massive PGE 2 in various tumors. Curcumin, a polyphenolic β-diketone from tumeric with anti-carcinogenic and anti-inflammatory activities, was shown to suppress PGE 2 formation and to block the expression of COX-2 and of microsomal PGE 2 synthase-1. Here, we identified microsomal PGE 2 synthase-1 as a molecular target of curcumin and we show that inhibition of microsomal PGE 2 synthase-1 activity is the predominant mechanism of curcumin to suppress PGE 2 biosynthesis. Curcumin reversibly inhibited the conversion of PGH 2 to PGE 2 by microsomal PGE 2 synthase-1 in microsomes of interleukin-1β-stimulated A549 lung carcinoma cells with an IC 50 of 0.2 to 0.3 μmol/L. Closely related polyphenols (e.g., resveratrol, coniferyl alcohol, eugenol, rosmarinic acid) failed in this respect, and isolated ovine COX-1 and human recombinant COX-2 were not inhibited by curcumin up to 30 μmol/L. In lipopolysaccharide-stimulated human whole blood, curcumin inhibited COX-2-derived PGE 2 formation from endogenous or from exogenous arachidonic acid, whereas the concomitant formation of COX-2-mediated 6-keto PGF 1 α and COX-1-derived 12(S)-hydroxy-5-cis-8,10-trans-heptadecatrienoic acid was suppressed only at significant higher concentrations. Based on the key function of PGE 2 in inflammation and carcinogenesis, inhibition of microsomal PGE 2 synthase-1 by curcumin provides a molecular basis for its anticarcinogenic and anti-inflammatory activities.

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“…Administration of curcumin (20-25 μM) inhibited the AA and PAF mediated platelet aggregation (Kim et al 2003;Lim et al 2004). It also mediates the AA-induced platelet aggregation and preferential inhibition of PAF showed suppressing effects on Ca 2+ signalling and TXA2 synthesis (Srivastava et al 1995).…”

Section: Antiplatelet Effect Of Curcuminmentioning

confidence: 99%

“…Antiplatelet effect Suppressed platelet-activating factor (PAF), ADP, epinephrine mediated platelet aggregation, collagen, and arachidonic acid (AA); Inhibited the AA and PAF mediated platelet aggregation Kim et al (2003); Lim et al (2004) Mediated the AA-induced platelet aggregation and preferential inhibition of PAF shows suppressing effects on and Ca 2+ signalling and TXA2 synthesis Srivastava et al (1995) Osteoprosis, osteoarthritis and akin disease Suppressed RANKL-induced osteoclastogenesis of rat monocyte-macrophage RAW264.7 cells Suda et al (1999) Induced the apoptosis in osteoclast rabbit, and inhibits the RANKL signalling and ultimately suppresses the RANKL-induced osteoclastogenesis in RAW 264.7 cells Ozaki et al (2000); Bharti et al (2004) Improved the bone microarchitecture and enhancing the mineral density in APP-PS1 transgenic rats Yang et al (2011) Significantly prevented from paw inflammation Ammon & Wahl (1991) Suppressed the COX-2 expression and also decreased the cellular protein kinases (JNK, protein kinase C), human epidermal growth factor receptors (EGFR & ErbB-2) and epidermal growth factor at the transcriptional level Goel et al (2001) Inhibited the NF-кB activation and hindered the c-jJun-AP-1 function Kim et al (2003) Decreased the expression of IL-6 and IL-8 pro-inflammatory cytokines Pol et al (2003) Showed inhibitory effect against different pro-inflammatory factors STAT3, NF-кB, and TNF Vamvouris & Hadi (2006); Abdou & Hanout (2008) Lowered the density of CD8+ T-cells and PK levels Heng et al (2000) Suppressed the keratinocyte proliferation and prevented from the posriais activity Pol et al (2003); Kurd et al (2008) Suppressed the lung fibroblasts through suppression of protein kinase C epsilon (PKC) Tourkina et al (2004) It induces apoptosis in scleroderma lung fibroblasts (SLFs) rats, and this effect was linked with the expression of PKC epsilon Xu et al (2007a) Suppressed GM-CSF, IL-4, and IL-5 production and inhibiting cytokines production that affect IgE synthesis, and eosinophil function Ram et al (2003) Inhibited the airway hyperreactivity, and OVA-induced airway constriction Yeon et al (2010) Kalpana and Menon (2004) stated that curcumin augmented an antioxidant defence system and modulated the biochemical marker enzymes. It also lowers the levels of free radicals and induction of detoxification enzymes and provides protection against life style related disorders (Manikandana et al 2004).…”

Section: Oxidative Stress and Curcuminmentioning

confidence: 99%

Curcumin and its allied analogues: epigenetic and health perspectives - a review

Imran¹,

Nadeem²,

Khan³

et al. 2017

Czech J. Food Sci.

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Curcumin (diferuoyl methane) is a yellow active ingredient present in turmeric. It is a homodimer of feruloylmethane that comprises a hydroxyl and methoxy group (heptadiene with two Michael acceptors), and α-, β-diketone. It contains various metabolites, i.e. hexahydrocurcumin (HHC), tetrahydrocurcumin (THC), octahydrocurcumin (OHC), dihydrocurcumin (DHC), curcumin sulphate, and curcumin glucuronide. Curcumin has been proven the most effective histone deacetylase (HDAC) inhibitor in HeLa nuclear extracts. It has the ability to affect the Akt, growth factors, NF-kB, and metastatic and angiogenic pathways. Curcumin has a strong therapeutic or preventive potential against several major human ailments, i.e. suppression of inflammation, cardiovascular, diabetes, tumorigenesis, chronic fatigue, antidepressant and neurological activities, depression, loss of muscle and bone, and neuropathic pain. In future, higher utilisation of curcumin as an active agent in food based products is required to curtail the human health disorders.

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Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets

Cited by 181 publications

References 14 publications

Mediterranean diet, but not red wine, is associated with beneficial changes in primary haemostasis

Mediterranean diet, but not red wine, is associated with beneficial changes in primary haemostasis

Curcumin blocks prostaglandin E2 biosynthesis through direct inhibition of the microsomal prostaglandin E2 synthase-1

Curcumin and its allied analogues: epigenetic and health perspectives - a review

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