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Hepatoprotective Effect of Amygdalin (Vit B17) Against Phenolphthalein Induced liver injury; involvement of Glial fibrillary acidic protein (GFAP)

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BackgroundPhenolphthalein (PTH) is an odorless and colorless chemical of laxative action and multiple side effects referred mostly to the production of free . It is primarily metabolized in the liver, hence its main adverse effects occur. Amygdalin (Vit B17) have antifibrotic, antiinflammatory and antitumor activities. The histopathological and functional changes in the liver together with the postulated protective hepatoprotective effect of Amygdalin were investigated in this study. Glial fibrillary acidic protein (GFAP) was considered as a marker of liver pathological changes.Material and methods30 adult male albino rats were divided into 3 groups. Group I was the control, group II received PTH alone and group III received both PTH and Amygdalin. At day 21, the levels of serum GFAP, total protein, total bilirubin and the activities of AST and ALT and liver hydroxyproline were estimated. The liver tissue samples were examined H&E, Masson’s trichrome and anti‐GFAP immunoreactive stains, and electron microscopic examination.ResultsThe liver enzymes, total bilirubin, hydroxyproline, and serum GFAP were significantly increased in group II compared with the control and in group III compared to group II. The total proteins were significantly decreased in group II in comparison to the controls and highly significantly increased in group III compared to group II. Group II showed disturbed hepatic architecture with extensive congestion, degeneration with inflammatory cell infiltration and marked collagen deposition. Group III showed preserved hepatic parenchyma and scanty inflammatory cells infiltration with decreased collagen. Group II had strong and diffuse immunoexpression and group III liver tissues were similar to the controls. The mean area percentage of GFAP immune staining showed a highly significant increased immunopositivity in group II when compared to the group I and a significant decsrease in group III compared to group II. The ultrastructure of hepatic stellate cells of group II showed dilated rough endoplasmic reticulum and loss of lipid droplets. Group III were similar to the controls.ConclusionAmygdalin treatment had a hepatoprotective effect against PTH induced liver injury and fibrosis and GFAP level could be a predictor for HSCs activation.Graphical AbstractFigure 1GFAP immune staining of the liver section of the control group (A) showing positive staining of the stellate cell and the endothelium of the sinusoids. The endothelium of the central veins is negatively stained. B: the PTH group showing strong and diffuse immunoexpression mostly perisinusoidal. C: The PTH‐Amg. group showed less marked dye expression. D: Diagram of the mean GFAP stained area percentage of the 3 animal groupsFigure 2
Title: Hepatoprotective Effect of Amygdalin (Vit B17) Against Phenolphthalein Induced liver injury; involvement of Glial fibrillary acidic protein (GFAP)
Description:
BackgroundPhenolphthalein (PTH) is an odorless and colorless chemical of laxative action and multiple side effects referred mostly to the production of free .
It is primarily metabolized in the liver, hence its main adverse effects occur.
Amygdalin (Vit B17) have antifibrotic, antiinflammatory and antitumor activities.
The histopathological and functional changes in the liver together with the postulated protective hepatoprotective effect of Amygdalin were investigated in this study.
Glial fibrillary acidic protein (GFAP) was considered as a marker of liver pathological changes.
Material and methods30 adult male albino rats were divided into 3 groups.
Group I was the control, group II received PTH alone and group III received both PTH and Amygdalin.
At day 21, the levels of serum GFAP, total protein, total bilirubin and the activities of AST and ALT and liver hydroxyproline were estimated.
The liver tissue samples were examined H&E, Masson’s trichrome and anti‐GFAP immunoreactive stains, and electron microscopic examination.
ResultsThe liver enzymes, total bilirubin, hydroxyproline, and serum GFAP were significantly increased in group II compared with the control and in group III compared to group II.
The total proteins were significantly decreased in group II in comparison to the controls and highly significantly increased in group III compared to group II.
Group II showed disturbed hepatic architecture with extensive congestion, degeneration with inflammatory cell infiltration and marked collagen deposition.
Group III showed preserved hepatic parenchyma and scanty inflammatory cells infiltration with decreased collagen.
Group II had strong and diffuse immunoexpression and group III liver tissues were similar to the controls.
The mean area percentage of GFAP immune staining showed a highly significant increased immunopositivity in group II when compared to the group I and a significant decsrease in group III compared to group II.
The ultrastructure of hepatic stellate cells of group II showed dilated rough endoplasmic reticulum and loss of lipid droplets.
Group III were similar to the controls.
ConclusionAmygdalin treatment had a hepatoprotective effect against PTH induced liver injury and fibrosis and GFAP level could be a predictor for HSCs activation.
Graphical AbstractFigure 1GFAP immune staining of the liver section of the control group (A) showing positive staining of the stellate cell and the endothelium of the sinusoids.
The endothelium of the central veins is negatively stained.
B: the PTH group showing strong and diffuse immunoexpression mostly perisinusoidal.
C: The PTH‐Amg.
group showed less marked dye expression.
D: Diagram of the mean GFAP stained area percentage of the 3 animal groupsFigure 2.

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