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Reviews |
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Sci Aging Knowledge Environ. 2004 Jul
14;2004(28):NF67
Resveratrol to the rescue
Leslie M.
A yeast is a worm is a fly is a person? At least the first three creatures
live longer when they sup an extract of red wine, according to new research.
The chemical activates related enzymes in all three organisms and might
duplicate the effects of extreme dieting. By showing for the first time
that the compound works in animals, the results bring human studies a step
closer. |
Int J Vitam Nutr Res. 2004 Mar;74(2):137-43
Red wine consumption prevents vascular oxidative stress
induced by a high-fat meal in healthy volunteers
Ventura P, Bini A, Panini R, Marri L, Tomasi A, Salvioli
G
Dept. of Internal Medicine, Section of Geriatrics and Gerontology, University
of Modena and Reggio Emilia, Italy
In order to investigate the effect of red wine on plasma lipid and oxidative
stress parameters after a high-fat meal, fifteen healthy volunteers were
studied: three days after a high-fat meal with 250 mL of water, they received
the same meal with 250 mL of red wine. During both periods, serial blood
samples were drawn before and 2, 4, and 8 hours after the meal to evaluate
plasma lipids (cholesterol and triglycerides; retinyl palmitate), oxidative
stress (D-ROM, and malondialdehyde) and antioxidant (total plasma antioxidant
levels and uric acid) parameters. During the meal without wine, plasma lipid
parameters increased significantly, whereas plasma total plasma antioxidant
levels decreased, and a trend toward reduction of uric acid levels was seen).
A similar trend in lipid parameters was observed after the meal with wine;
no significant difference in individual lipid parameter trends after a meal
with and without wine was observed. Wine ingestion induced higher total
plasma antioxidant levels and uric acid; malondialdehyde levels remained
constant after wine ingestion. Plasma D-ROM showed a significant postprandial
increase in both experiments, but it was significantly lowered after wine
ingestion. Our results give evidence of oxidative stress following a fat-rich
meal in healthy subjects, suggesting that ingestion of red wine during a
high-fat meal significantly reduces oxidative stress without inducing any
significant modification in postprandial lipemia. |
J Vasc Surg. 2004 Jul;40(1):138-45
Resveratrol, a red wine polyphenol, protects spinal
cord from ischemia-reperfusion injury
Kiziltepe U, Turan NN, Han U, Ulus AT, Akar F
Department of Cardiovascular Surgery, S.B. Dr. Muhittin Ulker Emergency
and Traumatology Hospital, Ankara, Turkey
OBJECTIVE: The cardioprotective effect of red wine has been attributed to
resveratrol. The resveratrol-induced protection against ischemia-reperfusion
(I/R) injury has been documented in heart, kidney, and brain. Resveratrol
scavenges free O(2) radicals and upregulates nitric oxide (NO). However,
the presence of resveratrol-induced spinal cord protection against I/R injury
has not been reported in the literature. The objective of this study was
to evaluate the effects of resveratrol on neurologic functions, histopathologic
changes, and NO metabolism following temporary spinal cord ischemia (SCI)
in rabbits.Material and methods SCI was induced with occlusion of the infrarenal
aorta in rabbits. In addition to the sham group (group S, n = 7), group
C (n = 7) received vehicle 30 minutes before ischemia. Group R1 (n = 7)
and R10 (n = 7) received 1 mg/kg and 10 mg/kg resveratrol instead of vehicle,
respectively. Blood samples were taken to obtain nitrite/nitrate levels
during the surgical procedure. After neurologic evaluation at the 48th hour
of reperfusion, lumbar spinal cords were removed for histopathologic examination
and malondialdehyde measurement as a marker of oxidative stress. RESULTS:
Five animals in group C had paraplegia while 5 in group R10 had normal neurologic
functions. The average Tarlov score of group R10 was significantly higher
than that the score of group C (4.1 +/- 1.2, vs 1.2 +/- 2.2; P =.014). Histopathologic
examination revealed higher neuronal viability index in group R10 compared
with that of group C (0.82 +/- 0.24 vs. 0.46 +/- 0.34; P =.018). Nitrite/nitrate
levels decreased in group C (from 357 +/- 20.15 micromol/L to 281 +/- 47.9
micromol/L; P <.01) whereas they increased both in group R1 and group
R10 (from 287+/-28 micromol/L to 310 +/- 33.9 micromol/L and from 296 +/-
106 micromol/L to 339 +/- 87 micromol/L, respectively) during SCI. Malondialdehyde
levels of group R10 was lower than those of group C (55 +/- 12.9 nmol/mg
protein vs 83.9 +/- 15.1 nmol/mg protein; P =.001, respectively). CONCLUSIONS:
In this model of SCI, resveratrol decreased oxidative stress, increased
NO release, and protected spinal cord from I/R injury. Resveratrol-induced
neuroprotection is probably mediated by its antioxidant and NO promoting
properties. Before considering the clinical use of this natural antioxidant,
further research is warranted about its mechanism of effects, timing, and
optimum dose. CLINICAL RELEVANCE: Paraplegia that results from spinal cord
ischemia is a catastrophic complication of thoracic and thoracoabdominal
aorta surgical procedures. Despite several surgical modifications and pharmacologic
approaches, paraplegia has not been totally eliminated. On clinical grounds,
the efficiency of currently used pharmacologic agents to prevent spinal
cord injury during thoracic and thoracoabdominal aorta surgery is very limited
and their benefit is controversial. Preischemic infusion of resveratrol
protects the spinal cord from ischemia reperfusion injury in rabbits. Following
clarification of the underlying protective mechanism, optimal dose, and
timing, resveratrol may used in humans as an adjunct to eliminate this catastrophic
complication. |
| Carcinogenesis. 2004
Jun 24
Resveratrol induces FasL-related apoptosis through
Cdc42 activation of ASK1/JNK-dependent signaling pathway in human leukemia
HL-60 cells
Su JL, Lin MT, Hong CC, Chang CC, Shiah SG, Wu CW, Chen
ST, Chau YP, Kuo ML
Laboratory of Molecular and Cellular Toxicology, Institute of Toxicology,
College of Medicine, National Taiwan University, Taipei, Taiwan
Trans-resveratrol, a phytoalexin found at high levels in grapes and in
grape products such as red wine, has been shown to prevent carcinogenesis
or anti-tumor growth in murine models. Here we dissect the detailed signaling
pathway involved in resveratrol-induced apoptosis. Our data showed that
treatment with resveratrol induced activation of apoptosis signal-regulating
kinase 1, a mitogen-activated protein kinase kinase kinase, in turn, activated
the downstream kinases c-Jun N-terminal kinase and p38 mitogen-activated
protein kinase, but not extracellular signal-regulated kinase. Transfection
with a dominant-negative c-Jun Nterminal kinase expression vector reduced
FasL expression and DNA fragmentation induced by resveratrol. However,
inhibition of p38 mitogen-activated protein kinase activity bytreatment
with SB203580 (p38 mitogen-activated protein kinase specific inhibitor)
or expression of mutant p38 mitogen-activated protein kinase expression
vector did not alter the apoptosis and FasL expression in response to
resveratrol. Furthermore, genetic inhibition of apoptosis signal-regulating
kinase 1 signaling inhibited not only the activation of c-Jun N-terminal
kinase, but also the expression of FasL and apoptosis. Similarly, over-expression
of wild type apoptosis signal-regulating kinase 1 strengthened the resveratrol-induced
c-Jun Nterminal kinase activation, FasL expression and subsequent apoptosis.
These results suggest the possible involvement of apoptosis signal-regulating
kinase 1/c-Jun N-terminal kinase signaling in the regulation of FasL expression
and subsequent apoptosis induced by resveratrol in HL-60 cells. Resveratrol
also activated the small GTP-binding protein Cdc42, rather than other
members such as RhoA or Rac1. Expression of a mutant Cdc42 (N17 Cdc42)
dramatically reduced resveratrol-induced JNK activity, FasL expression
and apoptotic cell death. These results showed that resveratrol induced
apoptosis through the Cdc42/ apoptosis signal-regulating kinase 1/c-Jun
N-terminal kinase/FasL signaling cascade in HL-60 cells. |
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RED WINE EXTRACT
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200 mg
red wine extract |
30 capsules |
USD 15.00 |
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