AIMS: To investigate the protective effect of Ginkgo biloba extract (GbE) on liver fibrosis induced by carbon tetrachloride (CCl4) in rats and expressions of transforming growth factor beta1 (TGF-beta1) and collagen I during this period. METHODS: The effect of GbE on liver fibrogenesis was detected by hematoxylin and eosin staining (H&E staining), Masson's trichrome staining, and electron microscope study. Blood samples were collected for measurement of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and albumin. Malondialdehyde (MDA) in liver tissue was detected by the thiobarbituric acid (TBA) method. Immunohistochemistry assay and RT-PCR were used to examine the protein expressions and mRNA levels of TGF-beta1 and collagen I, respectively. RESULTS: H&E, Masson's trichrome stainings and electron microscope study showed liver fibrosis in rats was greatly alleviated when treated with GbE. Additionally, there was a remarkable improvement of serum ALT, AST, albumin and MDA in the GbE-treated group. Immunohistochemistry and RT-PCR results showed GbE intervention significantly inhibited TGF-beta1 and collagen I expressions in rat liver. No side effects of GbE were found during these experiments. But GbE could not reverse the pathological changes of liver fibrosis completely when compared with normal control. CONCLUSION: GbE can partially protect rat liver from the fibrogenesis induced by CCl4. The mechanism may lie in its effect of inhibiting oxidative stress caused by liver injury and expressions of signal molecules such as TGF-beta1. GbE may thus be of potential help as a medicament or food additive for alleviation of liver fibrogenesis.
AIMS: To investigate the protective effect of Ginkgo biloba extract (GbE) on liver fibrosis induced by carbon tetrachloride (CCl4) in rats and expressions of transforming growth factor beta1 (TGF-beta1) and collagen I during this period. METHODS: The effect of GbE on liver fibrogenesis was detected by hematoxylin and eosin staining (H&E staining), Masson's trichrome staining, and electron microscope study. Blood samples were collected for measurement of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and albumin. Malondialdehyde (MDA) in liver tissue was detected by the thiobarbituric acid (TBA) method. Immunohistochemistry assay and RT-PCR were used to examine the protein expressions and mRNA levels of TGF-beta1 and collagen I, respectively. RESULTS: H&E, Masson's trichrome stainings and electron microscope study showed liver fibrosis in rats was greatly alleviated when treated with GbE. Additionally, there was a remarkable improvement of serum ALT, AST, albumin and MDA in the GbE-treated group. Immunohistochemistry and RT-PCR results showed GbE intervention significantly inhibited TGF-beta1 and collagen I expressions in rat liver. No side effects of GbE were found during these experiments. But GbE could not reverse the pathological changes of liver fibrosis completely when compared with normal control. CONCLUSION: GbE can partially protect rat liver from the fibrogenesis induced by CCl4. The mechanism may lie in its effect of inhibiting oxidative stress caused by liver injury and expressions of signal molecules such as TGF-beta1. GbE may thus be of potential help as a medicament or food additive for alleviation of liver fibrogenesis.
Authors: Florent Duval; Jorge E Moreno-Cuevas; María Teresa González-Garza; Carlos Rodríguez-Montalvo; Delia Elva Cruz-Vega Journal: Chin Med Date: 2014-12-24 Impact factor: 5.455