Overexpression of transforming growth factor beta 1 (TGF beta 1) and increased transcription of pro-collagen type I, are known to represent major events implicated in the development of liver fibrosis under either experimental or clinical conditions. Here we report that long-term dietary vitamin E supplementation in animals undergoing an experimental model of liver fibrosis (induced by chronic treatment of rats with carbon tetrachloride) results in a net inhibition of both hepatic TGF beta 1 and alpha 2 (I) procollagen mRNA levels. Moreover, of striking interest is the observation that vitamin E supplementation per so down-modulates basal levels of TGF beta 1 mRNA in the liver of untreated animals, suggesting that a dietary regimen rich in vitamin E may potentially interfere with both the initiation and progression of the fibrosclerotic processes.
Vitamin E dietary supplementation inhibits transforming growth factor beta 1 gene expression in the rat liver / M. Parola, R. Muraca, I. Dianzani, G. Barrera, G. Leonarduzzi, P. Bendinelli, R. Piccoletti, G. Poli. - In: FEBS LETTERS. - ISSN 0014-5793. - 308:3(1992 Aug 24), pp. 267-70-270.
Vitamin E dietary supplementation inhibits transforming growth factor beta 1 gene expression in the rat liver
P. Bendinelli;
1992
Abstract
Overexpression of transforming growth factor beta 1 (TGF beta 1) and increased transcription of pro-collagen type I, are known to represent major events implicated in the development of liver fibrosis under either experimental or clinical conditions. Here we report that long-term dietary vitamin E supplementation in animals undergoing an experimental model of liver fibrosis (induced by chronic treatment of rats with carbon tetrachloride) results in a net inhibition of both hepatic TGF beta 1 and alpha 2 (I) procollagen mRNA levels. Moreover, of striking interest is the observation that vitamin E supplementation per so down-modulates basal levels of TGF beta 1 mRNA in the liver of untreated animals, suggesting that a dietary regimen rich in vitamin E may potentially interfere with both the initiation and progression of the fibrosclerotic processes.Pubblicazioni consigliate
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