Resveratrol's antioxidant activity may play an important role in its possible cardioprotective action. Above, was mentioned its ability to inhibit the oxidation of LDL. Resveratrol also has been found to exert a strong inhibitory effect on superoxide anion and hydrogen peroxide production by macrophages stimulated by lipopolysaccharides or phorbol esters. It also has been demonstrated to decrease arachidonic acid release induced by lipopolysaccharides or phorbol esters, or by exposure to superoxide or hydrogen peroxide. It has hydroxyl-radical scavenging activity and has recently been found to possess glutathione-sparing activity.
In a rat study of the effect of resveratrol on ischemia-reperfusion, it was found that the substance had a dramatic effect against ischemia-reperfusion-induced arrhythmias and mortality. Resveratrol pretreatment both reduced the incidence and duration of ventricular dysrhythmias, including ventricular tachycardia and ventricular fibrillation. Resveratrol pretreatment also increased nitric oxide and decreased lactate dehydrogenase levels in the carotid blood. In this example, the cardioprotective effect of resveratrol may be correlated with its antioxidant activity, upregulation of nitric oxide synthesis and protection against endothelial dysfunction.
Resveratrol's possible phytoestrogenic activity may also contribute to its possible cardioprotective action. Resveratrol appears to act as a mixed agonist/antagonist for estrogen receptors alpha and beta. It has been found to bind estrogen receptor beta and estrogen receptor alpha with comparable affinity but with 7,000-fold lower affinity than estradiol. Resveratrol differs from other phytoestrogens, which bind estrogen receptor beta with higher affinity than they bind estrogen receptor alpha. Resveratrol also shows estradiol antagonistic behavior for estrogen receptor alpha with some estrogen receptors. It does not show estradiol antagonistic activity with estrogen receptor beta.
Resveratrol has demonstrated inhibition of growth of several cancer cell lines and tumors, suggesting that it has an inhibitory effect on cancer promotion/progression. It has been found to inhibit ribonucleotide reductase, DNA polymerase, the transcription of COX-2 in human mammary epithelial cells and the activity of ornithine decarboxylase. Ornithine decarboxylase is a key enzyme of polyamine biosynthesis, which is enhanced in tumor growth.
Resveratrol has also been found to induce phase II metabolizing enzymes which are involved in the detoxification of carcinogens, to upregulate apoptosis, to inhibit the progression of cancer by inducing cell differentiation and to inhibit protein kinase D and possibly protein kinase C. Recently, resveratrol has been shown to inhibit both NF-kappaB activation and NF-kappaB-dependent gene expression via its ability to inhibit IkappaB kinase activity, the key regulator of NF-kappaB activation. This appears to upregulate apoptosis.
It is clear that resveratrol has a wide range of activities that may account for its possible antiproliferative action. It is also clear that the mechanism of this possible action is far from being understood.
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