Resveratrol: A review of preclinical studies for human cancer prevention

Department of Dermatology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street VC15-204, New York, NY 10032, USA.
Toxicology and Applied Pharmacology (Impact Factor: 3.63). 12/2007; 224(3):274-83. DOI: 10.1016/j.taap.2006.12.025
Source: PubMed

ABSTRACT The search for novel and effective cancer chemopreventive agents has led to the identification of various naturally occurring compounds one of which is resveratrol (trans-3,4',5-trihydroxystilbene), a phytoalexin derived from the skin of grapes and other fruits. Resveratrol is known to have potent anti-inflammatory and antioxidant effects and to inhibit platelet aggregation and the growth of a variety of cancer cells. Its potential chemopreventive and chemotherapeutic activities have been demonstrated in all three stages of carcinogenesis (initiation, promotion, and progression), in both chemically and UVB-induced skin carcinogenesis in mice, as well as in various murine models of human cancers. Evidence from numerous in vitro and in vivo studies has confirmed its ability to modulate various targets and signaling pathways. This review discusses the current preclinical and mechanistic data available and assesses resveratrol's anticancer effects to support its potential as an anticancer agent in human populations.

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Available from: Mohammad Athar, Feb 11, 2015
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    • "Interestingly some natural products have shown synergistic effects with chemotherapeutic drugs and are also effective against multi drug resistance cancers (Athar et al., 2007; Gu et al., 2013; Liu and Chen, 2013). Boswellia ovalifoliolata (BO), an indigenous plant is mainly found in the areas of nilgiri hills of southern India. "
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    ABSTRACT: The present study was aimed at evaluation the apoptogenic potential of ethanolic extract of leaves from Boswellia ovalifoliolata (BL EthOH) and to explore the mechanism responsible for those activities implicated in Triple Negative Breast Cancer (TNBC) cells. BL EthOH was cytotoxic against TNBC cells like MDA-MB-231 and MDA-MB-453 with IC50 concentrations 67.48 ± 5.45 and 70.03 ± 4.76 μg/ml respectively. Apoptotic studies showed that BL EthOH was able to induce apoptosis and western blot studies demonstrated that BL EthOH significantly decreased the Phospho-NF-κB (ser536), PCNA, anti-apoptotic protein Bcl-2 expression and increased the expression of pro-apoptotic protein Bax, in MDA-MB-231 and MDA-MB-453 cell lines when compared with untreated cells. Besides, BL EthOH has synergistic chemosensitizing effects on TNBC cells and increased the cytotoxicity of doxorubicin and cisplatin.
    Environmental Toxicology and Pharmacology 07/2014; 38(1). DOI:10.1016/j.etap.2014.05.002 · 2.08 Impact Factor
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    • "Animal studies reporting beneficial effects of resveratrol in cancer have recently been published (Athar et al., 2007). "
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    ABSTRACT: The pleiotropic effects of resveratrol include anti-inflammatory, antioxidant and anti-cancer activities, and thus unique possibilities exist to explore mechanistic pathways of chemoprevention. The aim of this study was to investigate the role of miRNA alterations induced by resveratrol in the context of chemopreventive mechanisms against dextran sodium sulphate (DSS) induced colitis-associated tumorigenesis in the ApcMin/+ mouse. To that end, ApcMin/+ mice were exposed to 2% DSS to enhance intestinal inflammation and polyp development. Concurrently, mice received either vehicle or resveratrol treatment via oral gavage for five weeks. Interestingly, treatment of DSS-exposed mice with resveratrol resulted in decreased number and size of polyps, fewer histological signs of cell damage and decreased proliferating epithelial cells in intestinal mucosa compared to vehicle. Resveratrol treatment dramatically reversed the effects of DSS on the numbers of specific inflammatory CD4+ T cells, CD8+ T cells, B cells, natural killer T (NKT) cells and myeloid derived suppressor cells (MDSCs) in mesenteric lymph nodes. Resveratrol treatment also decreased IL-6 and TNF-α protein levels and reduced IL-6 and COX-2 mRNA expression. Microarray analysis revealed 104 microRNAs exhibiting greater than 1.5-fold differences in expression in the intestinal tissue of resveratrol treated mice. Among them, two microRNAs with anti-inflammatory properties, miRNA-101b and miRNA-455, were validated to be upregulated with resveratrol treatment by RT-PCR. Pathway analysis revealed that numerous differentially regulated miRNAs targeted mRNAs associated with inflammatory processes with known roles in intestinal tumorigenesis. These results suggest that resveratrol mediates anti-inflammatory properties and suppresses intestinal tumorigenesis through miRNA modulation.
    Journal of Pharmacology and Experimental Therapeutics 05/2014; 350(1). DOI:10.1124/jpet.114.213306 · 3.86 Impact Factor
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    • "RES has inhibitory effects in many types of cancer, e.g. prostate, lung, breast, colon, skin, and pancreatic cancers, leukemia, and lymphoma [13]. It may exert its anti-cancer action through activation of p53 and Bax, downregulation of Bcl2 and Bcl-XL [14] [15] [16], or inhibition of transcription of NF␬B, enhancing apoptosis via p53 activation [17]. "
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    ABSTRACT: This study investigated the effects of resveratrol (RES) on doxorubicin (DXR) induced rat bone marrow cell chromosome aberrations. RES, a polyphenolic compound, has attracted considerable attention because of its antioxidant and antimutagenic effects. DXR, a chemotherapeutic agent, is known to cause chromosomal aberrations in healthy cells in cancer patients. In this study, Wistar albino male rats were divided into 6 groups with 6 animals each. The control group received distilled water i.p. and the DXR group received an i.p. injection of doxorubicin (90mg/kg bw). For the 2 RES dose groups (12.5 and 25mg/kg bw respectively), RES was injected i.p. 5 times during the 24h study period to coincide with the schedule for the DXR+RES groups. The DXR-RES groups received DXR (90mg/kg bw) and RES at either 12.5 or 25mg/kg bw, i.p. 30min before, concurrently, and then every 6hours after DXR administration. Bone marrow collection was timed to coincide with 24hours after DXR administration in all groups. RES administration alone did not induce any significant increase in frequency of chromosome aberrations or abnormal metaphases compared with controls (p>0.05) while DXR alone did (p<0.05). In the DXR-RES 12.5mg/kg bw group, frequency of chromosome aberrations and abnormal metaphases were slightly reduced compared to DXR alone, but this was not statistically significant. However, in the DXR-RES 25mg/kg bw group, RES resulted in a statistically significant reduction in the frequency of chromosome aberrations and abnormal metaphases compared to those induced by DXR alone (p<0.05). These results indicate that RES (25mg/kg bw) significantly reduces frequency of DXR induced chromosome damage in bone marrow cells.
    Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 04/2014; DOI:10.1016/j.mrgentox.2014.03.008 · 4.44 Impact Factor
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