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Mangiferin relieves CCl4-induced liver fibrosis in mice
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Abstract
Background: Hepatic fibrosis is a late stage process of many chronic liver diseases. Blocking the fibrosis process will be beneficial to the treatment and recovery of the diseases. Mangiferin has many biological and pharmacological activities. Recently, it has been reported that mangiferin may relieve tissue fibrosis, including renal, myocardial, pulmonary fibrosis via anti-inflammatory and anti-oxidative effects in animal models.
Purpose: Here, we investigate the therapeutic effects of mangiferin on CCl4 induced liver fibrosis and the underlying mechanism in mice.
Materials/Methods: Thirty-two male C57BL/6 mice were randomly divided into 4 groups (n = 8 in each group), injected with carbon tetrachloride (10% CCl4) for 8 weeks and oral administrated with mangiferin (50 mg/kg or 100 mg/kg) from fifth week. The serum levels of ALT, AST were analyzed to evaluate liver function, H&E staining and Masson’s trichrome staining were used to assess liver morphology and the degree of liver fibrosis. Quantitative RT-PCR was used to assay the gene expression.
Results: Mangiferin alleviated the serum levels of AST, ALT, ALP, TBA and TBIL, reduced liver lesions, prevented hepatic parenchymal necrosis and ameliorated collagen accumulation in the liver of mice. Meanwhile, mangiferin inhibited the expression of inflammatory genes IL-6 and IL-1β, fibrogenic genes α-SMA, TGF-β and MMP-2 and bile acid metabolism genes ABCB4, ABCB11, SULT2A1 in the liver of CCl4-treated mice.
Conclusions: Our results suggest that mangiferin could alleviate liver fibrosis in CCl4-treated mice and mango consuming may have beneficial effects to hepatic fibrosis.
Title: Mangiferin relieves CCl4-induced liver fibrosis in mice
Description:
Abstract
Background: Hepatic fibrosis is a late stage process of many chronic liver diseases.
Blocking the fibrosis process will be beneficial to the treatment and recovery of the diseases.
Mangiferin has many biological and pharmacological activities.
Recently, it has been reported that mangiferin may relieve tissue fibrosis, including renal, myocardial, pulmonary fibrosis via anti-inflammatory and anti-oxidative effects in animal models.
Purpose: Here, we investigate the therapeutic effects of mangiferin on CCl4 induced liver fibrosis and the underlying mechanism in mice.
Materials/Methods: Thirty-two male C57BL/6 mice were randomly divided into 4 groups (n = 8 in each group), injected with carbon tetrachloride (10% CCl4) for 8 weeks and oral administrated with mangiferin (50 mg/kg or 100 mg/kg) from fifth week.
The serum levels of ALT, AST were analyzed to evaluate liver function, H&E staining and Masson’s trichrome staining were used to assess liver morphology and the degree of liver fibrosis.
Quantitative RT-PCR was used to assay the gene expression.
Results: Mangiferin alleviated the serum levels of AST, ALT, ALP, TBA and TBIL, reduced liver lesions, prevented hepatic parenchymal necrosis and ameliorated collagen accumulation in the liver of mice.
Meanwhile, mangiferin inhibited the expression of inflammatory genes IL-6 and IL-1β, fibrogenic genes α-SMA, TGF-β and MMP-2 and bile acid metabolism genes ABCB4, ABCB11, SULT2A1 in the liver of CCl4-treated mice.
Conclusions: Our results suggest that mangiferin could alleviate liver fibrosis in CCl4-treated mice and mango consuming may have beneficial effects to hepatic fibrosis.
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