Turmeric

Turmeric is referred as the “Queen of Spices”. It is loaded with many health nutrients and wide range of antioxidant and anti-inflammatory properties. This helps ward off dementia and reduce your risk of cancer. These antioxidants also maintain cholesterol levels and slow down the signs of normal aging.

CURCUMA

• Curcumina:• Antitrombotica

• Ipocolesterolemizzante

• Antiossidante

• Antinfiammatoria

• Blocca i tumori: leucemie, colon, seno

• Induce apoptosi e blocca l’angiogenesi

La Piperina (pepe) aumenta di 1000 volte l’assorbimento della Curcumina

CURCUMA LONGA

• Endurance exercise induces IL-6 production from myocytes that is thought to impair intracellular defence mechanisms. Curcumin inhibits NF-κB and activator protein 1, responsible for cytokine transcription, in cell lines. The aim of this study was to investigate the effect of curcumin supplementation on the cytokine and stress responses following 2 h of cycling.

RESEARCH ARTICLE Open Access

The effect of turmeric (Curcumin) supplementation on cytokine and inflammatory marker

responses following 2 hours of endurance cyclingJoseph N Sciberras1*, Stuart DR Galloway2, Anthony Fenech3, Godfrey Grech5, Claude Farrugia4,Deborah Duca4 and Janet Mifsud3

Sciberras et al. Journal of the International Society of Sports Nutrition (2015) 12:5

Dosage for the present study subjects was a single dose of 500 mg of Meriva® curcumin (5 tablets) with midday meal for three days, and then 500 mg ingested just before exercise. Samples for plasma curcumin analysis were taken at the final blood sampling time only in this study, three hours post ingestion to coincide with assessment of post-exercise interleukin response.

Carbohydrate and the cytokine response to 2.5 h of runningS. L. NEHLSEN-CANNARELLA,1 O. R. FAGOAGA,1 D. C. NIEMAN,2 D. A. HENSON,2D. E. BUTTERWORTH,2 R. L. SCHMITT,1 E. M. BAILEY,1 B. J. WARREN,2 A. UTTER,2AND J. M. DAVIS31Immunology Center and Department of Pathology, Loma Linda University Medical Center, Loma Linda, California 92350; 2Department of Health, Leisure, and Exercise Science and Department of Biology, Appalachian State University, Boone, North Carolina 28608; and 3Department of Exercise Science, School of Public Health, University of South Carolina, Columbia, South Carolina 29208

This randomized, double-blind, placebo-controlled study was designed to determine the influence of 6% carbohydrate (C) vs. placebo (P) beverage ingestion on cytokine responses (5 total samples over 9 h) to 2.5 h of high-intensity running (76.7 ± 0.4% maximal O2 uptake) by 30 experienced marathon runners.

For interleukin-6 (IL-6), a difference in the pattern of change between groups was found, highlighted by a greater increase in P vs. C immediately postrun (753 vs. 421%) and 1.5 h postrun (193 vs. 86%) [F(4,112) = 3.77,P = 0.006]. For interleukin-1-receptor antagonist (IL-1ra), a difference in the pattern of changebetween groups was found, highlighted by a greater increase in P vs. C 1.5 h postrun (231 vs. 72%) [F(2,50) = 6.38,P = 0.003]. No significant interaction effects were seen for bioactive IL-6 or IL-1β. The immediate postrun plasma glucose concentrations correlated negatively with those of plasma cortisol (r = −0.67, P < 0.001); postrun plasma cortisol (r = 0.70,P < 0.001) and IL-6 levels (r = 0.54,P = 0.003) correlated positively with levels of IL-1ra.

Taken together, the data indicate that carbohydrate ingestion attenuates cytokine levels in the inflammatory cascade in response to heavy exertion.

“Curcumina.., meglio se ad alta biodisponibilità”

Hypothesis!

NF-κB activation is a major

mediator of inflammation in

most diseases & inhibition of

NF-κB activation can

suppresses inflammation

Chronic obstructive pulmonary diseases

CancerHeart failure

Ischemia/ReperfusionArthritis AIDS

Asthma

Headache

Cardiac hypertrophy

Neuropathological disease

Helicobacter pylori-associated gastritis

Gut disease

Skin disease

Viral

infections

Sleep apnoea

Sepsis

Diabetes type 1 and II

Aging

LupusRenal disease

Incontinentia pigmenti

Ectodermal

dysplasia

Atherosclerosis

Multiple sclerosis

Muscular dystrophy

Alzheimer’s disease

Bone resorption

Crohn’s disease

NF-κB

NF-κB has been linked to several diseases

Systematic inflammatory response syndrome

Hypothesis!

> Most carcinogens activate NF- κB

> NF-κB activation mediates

carcinogenesis/tumorigenesis

> Inhibition of NF-κB activation

suppresses tumorigenesis

What activates NF-κB?

NF-κB

Stress(pH,

hypoxia,stres

s heavy

metals)Endotoxin

(LPS)

Carcinogens(e.g: TNF, CSC, DMBA)

Apoptosis-inducersChemotherapeutic agents &

γ-irradiation

Tumor Promoters(PMA)

Cytokines (TNF family, IL-1,

IL-17, IL-18, EGF)

Infection(bacterial/viral;

e.g HIV, EBV-LMP,

HTLV1)

ROI inducers(H2O2)

Aggarwal BB, Cancer Cell (in press)

What is NF-κB?

Cytoplasm

κB enhancer

Activator

p50 p65

IκBα

p50 p65 IκBαDegradation

p50 p65

Nucleus

Nuclear import

Ubiquitination &

Phosphorylation

IκBα

trasduzione del segnale attraverso IL-1RI e TNFR1. un | le due interleuchina 1 (IL-

agonisti 1 e IL-1 ) del segnale attraverso un recettore associata alla membrana (IL-1RI), che agisce di concerto con l'IL-1 proteina accessoria del recettore ( IL-1RAcP ) per avviare trasduzione del segnale. IL-1ra impedisce l'associazione di IL-1RI e IL-1RAcP. Formazione del complesso IL-1RI / IL-1RAcP, insieme con l'adattatore molecola MyD88 , porta al reclutamento della IL-1 chinasi recettore IRAK e IRAK2, che successivamente reclutare Recettore del fattore di necrosi tumorale (TNFR) Fattore -associated 6 (TRAF6) . Ciò porta all'attivazione di NF B e MAP-chinasi (MAPK) vie di segnalazione attraverso crescita trasformante factor (TGF ) chinasi -activated 1 (TAK1) e TAK1-binding protein (TAB1). Questa catena di eventi determina l'attivazione di fattori di trascrizione nucleare che successivamente indurre l'espressione di molti geni. b | L'attività biologica del fattore di necrosi tumorale (TNF ) è mediata da recettori del TNF 1 (TNFR1) e 2, che formano quando trimeri vincolato dal ligando. Attivazione di TNFR1 porta al reclutamento di TRAF2 / 5, RIP1 e FADD, attraverso la proteina adattatore TRADD . La successiva reclutamento e l'attivazione di caspasi 8 da FADD possono portare all'apoptosi. TRAF2 / 5 e RIP1 portano alla attivazione di NF B 'e AP-1 attraverso l'attivazione di IKK e MAPK. Così, TNF parti diverse vie di segnalazione a valle con IL-1. È importante notare che questa rappresentazione schematica non comprende tutte le informazioni disponibili su questi percorsi, ma serve come una semplice panoramica. AP-1, adattatore complesso proteico 1; Proteina con dominio morte FADD, Fas-associato; IKK, inducibile I B chinasi; JNK, c-Jun terminale N chinasi; MAP2Ks, MAPK chinasi; MAP3Ks, MAPK chinasi chinasi; MyD88, differenziazione mieloide gene risposta primaria, NIK, NF B inducono chinasi; p38, p38 MAPK; RIP1, recettore interagendo proteina 1; TRADD, proteine TNFR1-associato con il dominio della morte.

Role of NF-κB in Development of Cancer

NF-κB

Tumor promotione.g; COX2, iNOS, MMP-9, uPA

Metastasis

e.g; ICAM-1, VCAM-1, ELAM-1

Aggarwal BB, Cancer Cell (in press)

Immortalitye.g; telomerase

Anti-apoptosis/survival e.g; bcl-xl, cIAP, survivin, cFLIP,

TRAF, SOD, γ-GCS

Proliferatione.g; TNF, IL-1, IL-6

CyclinD1, cMyc

AngiogenesisVEGF, TNF, IL-1, IL-8

InflammationTNF, IL-1,Chemokines

NF-κB -regulated genes

Kumar A, Takada Y, Boriek AM, Aggarwal BB. Journal of Molecular Medicine 2004;82:434-48.

Possible site of action of curcumin on TNF- PMA- and H2O2-induced NF-kB activation.

Sanjaya Singh, and Bharat B. Aggarwal J. Biol. Chem.

1995;270:24995-25000

©1995 by American Society for Biochemistry and Molecular Biology