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    Resveratrol-poor red wines modulate SIRT1 in human renal cells.

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    The cardioprotective and anti-aging effects of red wine phenols, especially resveratrol (RSV), are well known. One of the most interesting biological properties of RSV and other naturally occurring phenols is the regulation of the expression and activity of SIRT1 (silent mating type information regulation 2 homolog). In view of the role of SIRT1 in acute and chronic renal diseases, we decided to study the effects of RSV-poor red wines on the expression of SIRT1 and HIF-2α (hypoxia-inducible factor 2α) to be compared with a nanomolar concentration of RSV or malvidin in proximal tubular cells of human kidneys (PTEC). Survival signaling systems activation (extracellular signal-regulated kinases, ERK and AMP-activated protein kinase, AMPK) was also investigated in PTEC incubated with wines. PTEC cells were incubated in the presence of RSV-poor wines diluted 1:1,000 for 30', 90', 120' and 24 h. Expression of SIRT1 and HIF-2α, and activation of ERK and AMPK were analyzed by Western Blot. The data obtained show that wine modulates the expression of anti-aging molecular systems even when RSV is present in very small amounts

    Cyclosporine-induced lipid peroxidation and propionyl carnitine protective effect

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    Cell and tissue lipoperoxidation of the kidney induced by cyclosporine through the release of reactive oxygen species has recently been pointed out to be one of the factors responsible for the toxic phenomena related to the administration of cyclosporine. Our previous research on propionyl carnitine had shown an antilipoperoxidative effect of this substance on isolated cells such as erythrocytes and leukocytes, and also on the endothelial, vasal and cardiac tissues. In the experiments presented herein we also examined if propionyl carnitine could carry out its already well-known antilipoperoxidative effect in the renal tissue, and if this mechanism could be taken into consideration in order to explain the protective effect of propionyl carnitine against cyclosporine induced toxicity. Trials were carried out on isolated and perfused rat kidneys, and we were able to observe that propionyl carnitine exerted a protective action on toxic lipid peroxidation phenomena induced by cyclosporine. The results we obtained, together with other mechanisms which we had already proved regarding the intense protective activity of propionyl carnitine on cyclosporine-induced nephrotoxicity, complete the complex picture that describes the protective activity of propionyl carnitine against cyclosporine toxicity
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