la curcuma

1. 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.

2. 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

3. CURCUMA LONGA

4. • 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 cycling
Joseph 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

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.

6. Carbohydrate and the cytokine response to 2.5 h of running
S. L. NEHLSEN-CANNARELLA,1 O. R. FAGOAGA,1 D. C. NIEMAN,2 D. A. HENSON,2
D. E. BUTTERWORTH,2 R. L. SCHMITT,1 E. M. BAILEY,1 B. J. WARREN,2 A. UTTER,2
AND J. M. DAVIS3
1Immunology 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 change
between 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.

9. “Curcumina..,
meglio se ad alta
biodisponibilità”

12. Hypothesis!
NF-κB activation is a major
mediator of inflammation in
most diseases & inhibition of
NF-κB activation can
suppresses inflammation

13. Chronic obstructive
pulmonary diseases
Cancer
Heart failure
Ischemia/Reperfusion
Arthritis 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

14. Hypothesis!
> Most carcinogens activate NF- κB
> NF-κB activation mediates
carcinogenesis/tumorigenesis
> Inhibition of NF-κB activation
suppresses tumorigenesis

15. What activates NF-κB?
NF-κB
Stress
(pH,
hypoxia,stres
s heavy
metals)
Endotoxin
(LPS)
Carcinogens
(e.g: TNF, CSC, DMBA)
Apoptosis-inducers
Chemotherapeutic 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)

16. What is NF-κB?
Cytoplasm
κB enhancer
Activator
p50 p65
IκBα
p50 p65 IκBα
Degradation
p50 p65
Nucleus
Nuclear import
Ubiquitination &
Phosphorylation
IκBα

17. 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.

18. Role of NF-κB in Development of Cancer
NF-κB
Tumor promotion
e.g; COX2, iNOS, MMP-9, uPA
Metastasis
e.g; ICAM-1, VCAM-1, ELAM-1
Aggarwal BB, Cancer Cell (in press)
Immortality
e.g; telomerase
Anti-apoptosis/survival
e.g; bcl-xl, cIAP, survivin, cFLIP,
TRAF, SOD, γ-GCS
Proliferation
e.g; TNF, IL-1, IL-6
CyclinD1, cMyc
Angiogenesis
VEGF, TNF, IL-1, IL-8
Inflammation
TNF, IL-1,Chemokines

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

20. 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