A genotypic association implicates myeloperoxidase in the progression of hepatic fibrosis in chronic hepatitis C virus infection

Reynolds, Wanda F.; Patel, Keyur; Pianko, Stephen; Blatt, Lawrence M.; Nicholas, John J.; McHutchison, John G.

doi:10.1038/sj.gene.6363880

Cited by 42 publications

(30 citation statements)

References 33 publications

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“…The production of these oxidants beside the cytokines will damage the hepatocytes and results in fibrosis [34]. Therefore, the antifibrotic action of hesperidin may in part be explained by its anti-inflammatory potential.…”

Section: Discussionmentioning

confidence: 99%

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

Abdel-sttar

Khalaf

Abo-Youssef

et al. 2017

Int J Pharm Pharm Sci

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Objective: Exposure to carbon tetrachloride leads to serious liver injury and fibrosis. This study was aimed to evaluate the hepatoprotective effects of hesperidin against carbon tetrachloride (CCl4)-induced liver fibrosis in rats compared with the reference drug silymarin.Methods: Wistar albino rats were divided into five groups, each of eight rats. Animals were allocated into a control group, corn oil group and fibrosis control group. The remaining two groups received in addition to CCl4, silymarin (100 mg/kg/d) as a reference treatment and hesperidin (200 mg/kg/d). At the end of experimental period, the biomarkers of specific fibrosis [hepatic transforming growth factor β1 (TGF-β1) and hydroxyproline (HYP)], liver function [serum alanine transaminase (ALT), aspartate transaminase (AST), albumin and total bilirubin], oxidative stress [hepatic malondialdehyde (MDA), glutathione (GSH) and catalase (CAT)], inflammatory [hepatic myeloperoxidase (MPO), serum tumor necrosis factor alpha (TNF-α)], relative liver weight, lipid profile [total cholesterol, serum triglycerides, high-density lipoprotein cholesterol (HDLCh) and low density lipoprotein cholesterol (LDL-Ch)] were evaluated, supported by liver histopathological study and immunohistochemistry of alpha-smooth muscle actin (α-SMA) in liver sections.Results: Hesperidin significantly decreased hepatic transforming growth factor β1, hydroxyproline, the serum liver function markers of ALT, AST and total bilirubin, the hepatic content of MDA and MPO activity, the serum pro-inflammatory cytokine TNF-α, relative liver weight, and the serum lipid profile markers cholesterol, triglycerides and LDL. On the other hand, Hesperidin significantly increased albumin, the hepatic content of GSH and CAT, and serum lipid profile of LDL. In addition, liver sections obtained from these groups showed marked histopathological and immunohistochemistry of α-SMA improvement. Conclusion:Hesperidin may be promising protective agent against liver fibrosis through improvement of liver function, modulation of the fibrous scar formation, anti-inflammatory and antioxidant potentials.

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Section: Discussionmentioning

confidence: 99%

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

Abdel-sttar

Khalaf

Abo-Youssef

et al. 2017

Int J Pharm Pharm Sci

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“…Prior studies have associated the GA/AA genotypes with an increased disease risk in subsets of cases with other inflammatory diseases, including Alzheimer's disease in aged Finnish males (16), lung cancer in aged Finnish males (28), and HCV-associated hepatic fibrosis (29).…”

Section: Figmentioning

confidence: 99%

−463 G/A Myeloperoxidase Promoter Polymorphism Is Associated with Clinical Manifestations and the Course of Disease in MPO-ANCA-Associated Vasculitis

Reynolds

Stegeman

Tervaert

2002

Clinical Immunology

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“…A functional upstream promoter polymorphism, Ϫ463GA, has been associated with expression levels (35,36), as well as incidence or severity of atherosclerosis (13,14), Alzheimer's (20, 38 -40), MPO-anti-neutrophil cytoplasmic antibodies vasculitis (41), hepatitis C virus-induced fibrosis (42), multiple sclerosis (43), periodontal disease (44), lung cancer (44,46), and myeloid leukemia (35). A number of studies report gender differences in association of Ϫ463GA with risk (20,38,40,41,44,46).…”

mentioning

confidence: 99%

Peroxisome Proliferator-activated Receptor γ Ligands Regulate Myeloperoxidase Expression in Macrophages by an Estrogen-dependent Mechanism Involving the -463GA Promoter Polymorphism

Kumar

Piedrafita

Reynolds

2004

Journal of Biological Chemistry

105

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A functional myeloperoxidase (MPO) promoter polymorphism, ؊463GA, has been associated with incidence or severity of inflammatory diseases, including atherosclerosis and Alzheimer's disease, and some cancers. The polymorphism is within an Alu element encoding four hexamer repeats recognized by nuclear receptors (AluRRE). Here we show that peroxisome proliferatoractivated receptor ␥ (PPAR␥) agonists strongly regulate MPO gene expression through the AluRRE. Opposite effects were observed in granulocyte/macrophage colony-stimulating factor (GMCSF)-versus macrophage colony-stimulating factor (

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A genotypic association implicates myeloperoxidase in the progression of hepatic fibrosis in chronic hepatitis C virus infection

Abstract: The hepatitis C virus (HCV) is a major cause of liver disease and the complications of cirrhosis. Liver biopsies

Cited by 42 publications

References 33 publications

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

−463 G/A Myeloperoxidase Promoter Polymorphism Is Associated with Clinical Manifestations and the Course of Disease in MPO-ANCA-Associated Vasculitis

Peroxisome Proliferator-activated Receptor γ Ligands Regulate Myeloperoxidase Expression in Macrophages by an Estrogen-dependent Mechanism Involving the -463GA Promoter Polymorphism

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