Chinese name: Pu Tao Zi
Medical Name: Semen vitis viniferae
Latin Name: Vitis vinifera
Taste: Sweet, tart
Quotes from Chinese historical sources
J Cell Biochem. 2009 Apr 22
Grape seed proanthocyanidins protect cardiomyocytes from ischemia and reperfusion injury via Akt-NOS signaling.
Shao ZH, Wojcik KR, Dossumbekova A, Hsu C, Mehendale SR, Li CQ, Qin Y, Sharp WW, Chang WT, Hamann KJ, Yuan CS, Hoek TL.
Department of Medicine, Emergency Resuscitation Center, Section of Emergency Medicine, University of Chicago, Chicago, Illinois 60637.
Ischemia/reperfusion (I/R) injury in cardiomyocytes is related to excess reactive oxygen species (ROS) generation and can be modulated by nitric oxide (NO). We have previously shown that grape seed proanthocyanidin extract (GSPE), a naturally occurring antioxidant, decreased ROS and may potentially stimulate NO production. In this study, we investigated whether GSPE administration at reperfusion was associated with cardioprotection and enhanced NO production in a cardiomyocyte I/R model. GSPE attenuated I/R-induced cell death [18.0 +/- 1.8% (GSPE, 50 microg/ml) vs. 42.3 +/- 3.0% (I/R control), P < 0.001], restored contractility (6/6 vs. 0/6, respectively), and increased NO release. The NO synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME, 200 microM) significantly reduced GSPE-induced NO release and its associated cardioprotection [32.7 +/- 2.7% (GSPE + L-NAME) vs. 18.0 +/- 1.8% (GSPE alone), P < 0.01]. To determine whether GSPE induced NO production was mediated by the Akt-eNOS pathway, we utilized the Akt inhibitor API-2. API-2 (10 microM) abrogated GSPE-induced protection [44.3% +/- 2.2% (GSPE + API-2) vs. 27.0% +/- 4.3% (GSPE alone), P < 0.01], attenuated the enhanced phosphorylation of Akt at Ser473 in GSPE-treated cells and attenuated GSPE-induced NO increases. Simultaneously blocking NOS activation (L-NAME) and Akt (API-2) resulted in decreased NO levels similar to using each inhibitor independently. These data suggest that in the context of GSPE stimulation, Akt may help activate eNOS, leading to protective levels of NO. GSPE offers an alternative approach to therapeutic cardioprotection against I/R injury and may offer unique opportunities to improve cardiovascular health by enhancing NO production and increasing Akt-eNOS signaling. J. Cell. Biochem. (c) 2009 Wiley-Liss, Inc.
Neurotox Res. 2009 Jan;15(1):3-14.
Consumption of Grape Seed Extract Prevents Amyloid-beta Deposition and Attenuates Inflammation in Brain of an Alzheimer's Disease Mouse
Wang YJ, Thomas P, Zhong JH, Bi FF, Kosaraju S, Pollard A, Fenech M, Zhou XF.
Department of Human Physiology and Centre for Neuroscience, Flinders University, GPO Box 2100, Adelaide, SA, Australia.
Polyphenols extracted from grape seeds are able to inhibit amyloid-beta (Abeta) aggregation, reduce Abeta production and protect against Abeta neurotoxicity in vitro. We aimed to investigate the therapeutic effects of a polyphenol-rich grape seed extract (GSE) in Alzheimer's disease (AD) mice. APP(Swe)/PS1dE9 transgenic mice were fed with normal AIN-93G diet (control diet), AIN-93G diet with 0.07% curcumin or diet with 2% GSE beginning at 3 months of age for 9 months. Total phenolic content of GSE was 592.5 mg/g dry weight, including gallic acid (49 mg/g), catechin (41 mg/g), epicatechin (66 mg/g) and proanthocyanidins (436.6 mg catechin equivalents/g). Long-term feeding of GSE diet was well tolerated without fatality, behavioural abnormality, changes in food consumption, body weight or liver function. The Abeta levels in the brain and serum of the mice fed with GSE were reduced by 33% and 44%, respectively, compared with the Alzheimer's mice fed with the control diet. Amyloid plaques and microgliosis in the brain of Alzheimer's mice fed with GSE were also reduced by 49% and 70%, respectively. Curcumin also significantly reduced brain Abeta burden and microglia activation. Conclusively, polyphenol-rich GSE prevents the Abeta deposition and attenuates the inflammation in the brain of a transgenic mouse model, and this thus is promising in delaying development of AD.
Anticancer Res. 2009 Jan;29(1):283-9
Mechanisms of grape seed procyanidin-induced apoptosis in colorectal carcinoma cells.
Hsu CP, Lin YH, Chou CC, Zhou SP, Hsu YC, Liu CL, Ku FM, Chung YC.
Department of Medical Technology, Yuanpei University, Hsinchu, Taiwan.
BACKGROUND: Grape seed procyanidins (GSP) can inhibit cell proliferation and tumorigenesis, and induce apoptosis in human breast, prostate, skin and colorectal carcinoma cell lines. MATERIALS AND METHODS: In order to study the mechanism of apoptosis, four colorectal cell lines, HT-29, SW-480, LoVo and Colo 320DM, were used. GSP-treated cells were assessed for viability by trypan blue exclusion, for loss of mitochondrial membrane potential by rhodamine 123 staining, for increased apoptosis by annexin V labeling, and for changes in the levels of proteins involved in apoptosis by immunoblotting. RESULTS: GSP had no significant pro-apoptotic effect on the Colo 320DM cell line. In HT-29, SW-480 and LoVo cells, GSP (12.5-50 mg/l) inhibited proliferation in a dose-dependent manner. In these three lines, GSP treatment increased the proportion of rhodamine 123-negative cells and annexin V-positive cells, while immunoblotting revealed increased levels of apoptosis activation protein, caspase-3 and the cleavage fragment of PARP (a caspase-3 substrate), but the level of Bcl-2 did not change. CONCLUSION: GSP inhibited the proliferation of some colorectal carcinoma cell lines and was associated with an apoptotic mechanism involving a loss of mitochondrial membrane potential and caspase-3 activation in these cells.
Food Chem Toxicol. 2009 Feb 20
Inhibition of inflammatory mediators by polyphenolic plant extracts in human intestinal Caco-2 cells
Romier-Crouzet B, Van De Walle J, During A, Joly A, Rousseau C, Henry O, Larondelle Y, Schneider YJ.
Biochimie Cellulaire, Nutritionnelle et Toxicologique, Institut des Sciences de la Vie, Université Catholique de Louvain, Croix du Sud, 5, B 1348 Louvain-la-Neuve, Belgium.
The mitogen-activated protein kinases (MAPK) and nuclear factor kappaB (NF-kappaB) are involved in transduction cascades that play a key role in inflammatory response. We tested the ability of preselected natural polyphenolic extracts (grape seed, cocoa, sugar cane, oak, mangosteen and pomegranate) to modulate intestinal inflammation using human intestinal Caco-2 cells treated for 4h with these extracts and then stimulated by cytokines for 24 or 48h. The effect of polyphenolic extracts, at 50mumol of gallic acid equivalent/l, was investigated on inflammation-related cellular events: (i) NF-kappaB activity (cells transfected with a NF-kappaB-luciferase construct), (ii) activation of Erk1/2 and JNK (western blotting), (iii) secretion of interleukin 8 (IL-8) (ELISA), (iv) secretion of prostaglandin (PG) E(2) (ELISA), (v) production of NO (Griess method). Results show that: (i) sugar cane, oak and pomegranate extracts inhibited NF-kappaB activity (from 1.6 to 1.9-fold) (P<0.001); (ii) pomegranate slightly inhibited Erk1/2 activation (1.3-fold) (P=0.008); (iii) oak and pomegranate decreased NO synthesis by 1.5-fold (P<0.001) and that of IL-8 by 10.3 and 6.7-fold respectively; (iv) pomegranate and cocoa decreased PGE(2) synthesis by 4.6 (P<0.0001) and 2.2-fold (P=0.001), respectively. We suggest that pomegranate extract could be particularly promising in dietary prevention of intestinal inflammation.