Comparative Studies of the Antioxidant Effects of Cis- and Trans- Resveratrol

Orallo, Francisco

doi:10.2174/092986706775197962

Cited by 184 publications

(97 citation statements)

References 16 publications

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“…This effect is inhibited by t-RESV, but not by c-RESV, and similar results are observed in postcapillary venules. Although a number of in vitro studies have revealed quantitative differences in the activity of the two forms, with the cis isomer appearing to be less active than its trans isomer (34)(35)(36), to our knowledge this is the first report to show that t-RESV inhibits the leukocyte-endothelial cell interactions induced by Ang-II in vivo, whereas c-RESV does not. Based on this finding, t-RESV was used in all subsequent experiments to elucidate and characterize the cardiovascular effects of RESV.…”

Section: Discussionmentioning

confidence: 71%

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Trans- but Not Cis-Resveratrol Impairs Angiotensin-II–Mediated Vascular Inflammation through Inhibition of NF-κB Activation and Peroxisome Proliferator-Activated Receptor-γ Upregulation

Rius¹,

Abu-Taha²,

Hermenegildo

et al. 2010

The Journal of Immunology

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Angiotensin II (Ang-II) displays inflammatory activity and is implicated in several cardiovascular disorders. This study evaluates the effect of cis- and trans (t)-resveratrol (RESV) in two in vivo models of vascular inflammation and identifies the cardioprotective mechanisms that underlie them. In vivo, Ang-II–induced arteriolar leukocyte adhesion was inhibited by 71% by t-RESV (2.1 mg/kg, i.v.), but was not affected by cis-RESV. Because estrogens influence the rennin-angiotensin system, chronic treatment with t-RESV (15 mg/kg/day, orally) inhibited ovariectomy-induced arteriolar leukocyte adhesion by 81%, partly through a reduction of cell adhesion molecule (CAM) expression and circulating levels of cytokine-induced neutrophil chemoattractant, MCP-1, and MIP-1α. In an in vitro flow chamber system, t-RESV (1–10 μM) undermined the adhesion of human leukocytes under physiological flow to Ang-II–activated human endothelial cells. These effects were accompanied by reductions in monocyte and endothelial CAM expression, chemokine release, phosphorylation of p38 MAPK, and phosphorylation of the p65 subunit of NF-κB. Interestingly, t-RESV increased the expression of peroxisome proliferator-activated receptor-γ in human endothelial and mononuclear cells. These results demonstrate for the first time that the in vivo anti-inflammatory activity of RESV is produced by its t-RESV, which possibly interferes with signaling pathways that cause the upregulation of CAMs and chemokine release. Upregulation of proliferator-activated receptor-γ also appears to be involved in the cardioprotective effects of t-RESV. In this way, chronic administration of t-RESV may reduce the systemic inflammatory response associated with the activation of the rennin-angiotensin system, thereby decreasing the risk of further cardiovascular disease.

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Section: Discussionmentioning

confidence: 71%

“…RESV can act on NAD (NADPH)-dependent oxidases, hypoxanthine/xanthine oxidase, 15-lipoxygenase, myeloperoxidase, and NO synthases (35,44). Its actions on these enzymes contribute to a reduction in the formation of intracellular reactive oxygen species (ROS).…”

Section: Discussionmentioning

confidence: 99%

Trans- but Not Cis-Resveratrol Impairs Angiotensin-II–Mediated Vascular Inflammation through Inhibition of NF-κB Activation and Peroxisome Proliferator-Activated Receptor-γ Upregulation

Rius¹,

Abu-Taha²,

Hermenegildo

et al. 2010

The Journal of Immunology

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“…Res, a kind of non-flavonoid polyphenol, found in black grapes and red wine, is characterized as a phytoalexin and is produced by a variety of plants in response to stress. It was used as a natural plant compound in traditional Chinese and Japanese medicine (8,9). Recently, it has been reported that Res can inhibit proliferation and promote apoptosis of various types of cancer cells, such as pancreas, breast and colon cancer (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol inactivates PI3K/Akt signaling through upregulating BMP7 in human colon cancer cells

et al. 2017

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Abstract. Colon cancer is common worldwide and accounts for the significant cancer related morbidity and mortality in patients. Although extensive advancement has been made in colon cancer treatment and diagnosis in the last decades, there is still a giant gap between the clinical expectation. It has been reported that resveratrol (Res) may be a potential candidate for cancer treatment. However, the specific mechanism underlying this activity remains unclear. In this study, we investigated the anticancer activity of Res in human colon cancer cells, and unveiled the possible mechanism for this effect. With cell viability, flow cytometry, PCR and western blot analysis, we demonstrated the efficacious anticancer activity of Res in HCT116 cells. Mechanically, we found that Res greatly upregulates BMP7 in HCT116 cells. Exogenous BMP7 enhances the anticancer effect of Res in HCT116 cells, which was almost reversed by the BMP7 specific antibody. Res does not activate the BMPs/Smads signaling, but decreases the phosphorylation of Akt1/2/3 substantially in HCT116 cells. Exogenous BMP7 enhances the inhibitory effect of Res on the phosphorylation of Akt1/2/3, while BMP7 immunodepletion reverses this effect notably. Res markedly decreases the phosphorylation of PTEN, which can be enhanced by exogenous BMP7 but partly reversed by the BMP7 antibody. Our findings suggested that Res may be a promising candidate for colon cancer treatment, and the anticancer activity may be mediated by inactivating PI3K/Akt signaling through upregulating BMP7 to decrease, at least, the phosphorylation of

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“…Resveratrol, a polyphenol found in berries, nuts, and red wine, has a variety of cancer chemopreventive activities including anti-inflammatory, pro-apoptotic, anti-angiogenic, and chemosensitizing properties in a variety of cultured cells and in vivo systems (10). Although resveratrol is redox active and has been claimed to be an antioxidant (11), reports also show the pro-oxidant capacity of resveratrol (12,13). Piperine, a main component of Piper longum Linn.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol and piperine enhance radiosensitivity of tumor cells

Tak¹,

Lee²,

Park³

2012

BMB Reports

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The use of ionizing radiation (IR) is essential for treating many human cancers. However, radioresistance markedly impairs the efficacy of tumor radiotherapy. IR enhances the production of reactive oxygen species (ROS) in a variety of cells which are determinant components in the induction of apoptosis. Much interest has developed to augment the effect of radiation in tumors by combining it with radiosensitizers to improve the therapeutic ratio. In the current study, the radiosensitizing effects of resveratrol and piperine on cancer cells were evaluated. Cancer cell lines treated with these natural products exhibited significantly augmented IR-induced apoptosis and loss of mitochondrial membrane potential, presumably through enhanced ROS generation. Applying natural products as sensitizers for IR-induced apoptotic cell death offers a promising therapeutic approach to treat cancer. [BMB reports 2012; 45(4): 242-246]

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Comparative Studies of the Antioxidant Effects of Cis- and Trans- Resveratrol

Cited by 184 publications

References 16 publications

Trans- but Not Cis-Resveratrol Impairs Angiotensin-II–Mediated Vascular Inflammation through Inhibition of NF-κB Activation and Peroxisome Proliferator-Activated Receptor-γ Upregulation

Trans- but Not Cis-Resveratrol Impairs Angiotensin-II–Mediated Vascular Inflammation through Inhibition of NF-κB Activation and Peroxisome Proliferator-Activated Receptor-γ Upregulation

Resveratrol inactivates PI3K/Akt signaling through upregulating BMP7 in human colon cancer cells

Resveratrol and piperine enhance radiosensitivity of tumor cells

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