The effect of vitamin A on CCl4-induced hepatic injuries in rats: a histochemical, immunohistochemical and ultrastructural study


Noyan S., Cavusoglu I., Minbay F. Z.

ACTA HISTOCHEMICA, vol.107, no.6, pp.421-434, 2006 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 107 Issue: 6
  • Publication Date: 2006
  • Doi Number: 10.1016/j.acthis.2005.09.001
  • Journal Name: ACTA HISTOCHEMICA
  • Journal Indexes: Science Citation Index Expanded, Scopus
  • Page Numbers: pp.421-434
  • Keywords: Ito celts, vitamin A, desmin, alpha-smooth muscle actin, alpha-SMA, FAT-STORING CELLS, ALCOHOLIC LIVER-INJURY, SMOOTH-MUSCLE-ACTIN, ITO-CELLS, CARBON-TETRACHLORIDE, PERISINUSOIDAL CELLS, EXTRACELLULAR-MATRIX, TRANSITIONAL CELLS, COLLAGEN TYPES, FIBROSIS

Abstract

In this study, we aimed to investigate the effect of vitamin A on the transformation of the Ito cells to fibrogenic form and suppression of the development of fibrosis. Carbon tetrachloride intoxication was performed on rats for 2, 8, 12 or 20 weeks and 5 x 10(4) IU vitamin A (as retinol palmitate) was injected subcutaneously once every 4 weeks. Ito cells were detected by gold chloride impregnation, as well as desmin and alpha-smooth muscle actin (alpha-SMA) immunohistochemistry. Additionally, all groups were examined ultrastructurally. The number of Ito cells that were labelled positively with gold impregnation decreased in the fibrotic groups; however, alpha-SMA and desmin immunopositive Ito cells increased. The samples from animals that were treated with vitamin A showed an increase in labelling with gold impregnation but a decrease in alpha-SMA immunopositivity. The data showed that vitamin A can prevent hepatic injury, by suppressing the transformation of Ito cells to fibrogenic form. We conclude that vitamin A has potential for the treatment of hepatic fibrotic diseases. alpha-SMA immunohistochemistry was found to be more informative than desmin immunohistochemistry for monitoring Liver fibrosis. (c) 2005 Elsevier GmbH. All rights reserved.