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

Noyan, Semiha; Çavuşoğlu, İlkin; Minbay, Fatma

doi:10.1016/j.acthis.2005.09.001

Cited by 22 publications

(10 citation statements)

References 33 publications

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“…Beta-carotene, a precursor of retinol, was shown to cause a milder pathological phenotype in a rat model of CCl4-induced hepatic fibrosis when compared to untreated controls [36]. Consistently, retinol administration prevented liver fibrosis induced by CCl4 by suppressing HSCs activation [34,37], and retinyl palmitate treatment in rats injured with dimethylnitrosamine or with pig serum decreased the number of activated HSCs thereby preventing collagen deposition and fibrosis in liver [33]. The all-trans RA isomer was found to alleviate ethanol-induced liver damage [35].…”

Section: Hepatic Stellate Cells Activation and Retinoic Acidmentioning

confidence: 73%

“…Studies on cultured cells showed retinoids to inhibit HSCs proliferation and activation [29][30][31][32]. In vivo studies demonstrated that the administration of retinol or its derivatives decreases liver fibrosis in different experimental models [33][34][35][36][37]. Beta-carotene, a precursor of retinol, was shown to cause a milder pathological phenotype in a rat model of CCl4-induced hepatic fibrosis when compared to untreated controls [36].…”

Section: Hepatic Stellate Cells Activation and Retinoic Acidmentioning

confidence: 99%

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Senescence in hepatic stellate cells as a mechanism of liver fibrosis reversal: a putative synergy between retinoic acid and PPAR-gamma signalings

et al. 2016

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Hepatic stellate cells (HSCs), also known as perisinusoidal cells, are pericytes found in the perisinusoidal space of the liver. HSCs are the major cell type involved in liver fibrosis, which is the formation of scar tissue in response to liver damage. When the liver is damaged, stellate cells can shift into an activated state, characterized by proliferation, contractility and chemotaxis. The activated HSCs secrete collagen scar tissue, which can lead to cirrhosis. Recent studies have shown that in vivo activation of HSCs by fibrogenic agents can eventually lead to senescence of these cells, which would contribute to reversal of fibrosis although it may also favor the insurgence of liver cancer. HSCs in their non-active form store huge amounts of retinoic acid derivatives in lipid droplets, which are progressively depleted upon cell activation in injured liver. Retinoic acid is a metabolite of vitamin A (retinol) that mediates the functions of vitamin A, generally required for growth and development. The precise function of retinoic acid and its alterations in HSCs has yet to be elucidated, and nonetheless in various cell types retinoic acid and its receptors (RAR and RXR) are known to act synergistically with peroxisome proliferator-activated receptor gamma (PPAR-gamma) signaling through the activity of transcriptional heterodimers. Here, we review the recent advancements in the understanding of how retinoic acid signaling modulates the fibrogenic potential of HSCs and proposes a synergistic combined action with PPAR-gamma in the reversal of liver fibrosis.

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Section: Hepatic Stellate Cells Activation and Retinoic Acidmentioning

confidence: 73%

Section: Hepatic Stellate Cells Activation and Retinoic Acidmentioning

confidence: 99%

Senescence in hepatic stellate cells as a mechanism of liver fibrosis reversal: a putative synergy between retinoic acid and PPAR-gamma signalings

et al. 2016

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“…Several studies reported hepatic centrilobular steatosis and necrosis after exposure to CCl 4 . 4,[37][38][39][40][41] The changes in organelle structure and edematous cytoplasmic matrix in this group were probably due to the changes in membrane structure caused by lipid peroxidation. Especially, the changes that we have seen in rough endoplasmic reticulum structure such as granular loss and disruption of the cisternal structure were signs of membrane structure damage.…”

Section: Discussionmentioning

confidence: 86%

Protective effects of ascorbic acid on hepatotoxicity and oxidative stress caused by carbon tetrachloride in the liver of Wistar rats

Ozturk

Öztürk

Gül

et al. 2009

Cell Biochemistry & Function

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This study was planned to investigate the protective effect of l(+)-ascorbic acid (Vit C) on CCl(4)-induced hepatotoxicity and oxidative stress in the liver of Wistar rats (Rattus Norvegicus, strain Wistar). Twenty-four adult male Wistar rats were fed with standard rat chow diet for 10 days and randomly were divided into four groups of six each as follows: (1) control, (2) CCl(4), (3) "CCl(4) + Vit C", (4) Vit C groups. CCl(4) was applied to rats belonging to CCl(4) and "CCl(4) + Vit C" groups subcutaneously at 1 mg kg(-1) dose CCl(4) for 3 days. Vit C applied to "CCl(4) + Vit C" and "Vit C" group rats intraperitoneally at 300 mg kg(-1) dose for 3 days. All rats were sacrificed and livers were quickly removed on the fourth day of the experiment. MDA, total glutathione (T.GSH) levels and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) activities were measured in the liver of all groups of rats and also serum alanine amino transferase (ALT) and aspartate amino transferase (AST) activities were detected to determine liver functions in all groups of rats. Histopathological changes were evaluated by light and transmission electron microscopes. In "CCl(4) + Vit C" group, MDA level was significantly decreased (p < 0.05) and SOD, CAT, GSH-PX activities were significantly increased (p < 0.005, 0.01, 0.05) respectively, T.GSH level was significantly increased (p < 0.005) and serum ALT and AST activities were significantly decreased (p < 0.01, 0.05), respectively, when compared with CCl(4) group. These results show that Vit C has a highly protective effect on hepatotoxicity and oxidative stress caused by CCl(4).

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“…Several studies have shown that vitamin A content is depleted in the fibrotic and cirrhotic stages (Leo & Lieber, 1982; Yamane et al. , 1993; Noyan et al. , 2006).…”

Section: Introductionmentioning

confidence: 99%

The effectiveness of relative dose response to retinol intake as an evaluation of vitamin A status of cirrhotic patients

Paula

Ramalho

Braulio

2010

J Human Nutrition Diet

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

Cited by 22 publications

References 33 publications

Senescence in hepatic stellate cells as a mechanism of liver fibrosis reversal: a putative synergy between retinoic acid and PPAR-gamma signalings

Senescence in hepatic stellate cells as a mechanism of liver fibrosis reversal: a putative synergy between retinoic acid and PPAR-gamma signalings

Protective effects of ascorbic acid on hepatotoxicity and oxidative stress caused by carbon tetrachloride in the liver of Wistar rats

The effectiveness of relative dose response to retinol intake as an evaluation of vitamin A status of cirrhotic patients

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