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Effect of Gallic Acid on Regression of Murine CCL4-Induced Hepatic Cirrhosis

Received: 26 September 2016     Accepted: 19 October 2016     Published: 15 January 2017
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Abstract

Hepatic cirrhosis can be induced by chronic exposure to reactive oxygen species (ROS). However, phenolic compounds, such as gallic acid (GA), appear to inhibit ROS-induced oxidative stress. We aimed to investigate the effects of GA on murine hepatic fibrogenesis. The effects of GA were evaluated on the regression of liver cirrhosis that was induced by chronic intraperitoneal CCl4 administration (20% v/v) in C57 mice for a period of 10 weeks. The animals were treated intraperitoneally and distributed in three groups, as follows: SHAM group – 8 weeks with Olive oil (CCL4 solution vehicle); C group – 8 weeks with CCL4 solution, and then 2 more weeks with deionized water (Gallic Acid solution vehicle); and C + GA group – 8 weeks with CCL4 solution, and then 2 more weeks with Gallic Acid solution (100 mg/Kg/day) on alternated days. The cirrhosis and inflammation-related factors were estimated using histological, western blotting and PCR-RT analysis. There was a significant decrease in the collagen deposition, as indicated by Sirius red staining, in the C + GA group compared to the C group (p<0.05). This improvement was accompanied by a reduction in the number of α-SMA-positive cells observed in these animals (p<0.05). The expression of the Procollagen α1(I), TGFβ1 and TIMP1 genes was also diminished by GA administration compared to the control (p<0.001). Additionally, proteomic studies revealed reduced p65 NFκB and p38 MAPK protein levels in the C + GA group. These findings reveal the effect of GA on the regression of cirrhosis. The mechanisms of this process might involve the anti-inflammatory activity of GA, which represses the TGFβ1, p65 NFκB, and p38 MAPK-mediated signaling pathways.

Published in International Journal of Homeopathy & Natural Medicines (Volume 2, Issue 1)
DOI 10.11648/j.ijhnm.20160201.13
Page(s) 15-19
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2017. Published by Science Publishing Group

Keywords

Phenolic Compounds, Gallic Acid, Liver Cirrhosis, Oxidative Stress, Reactive Oxygen Species, Hepatic Stellate Cells

References
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Cite This Article
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    Sérgio Souza Figueiredo, Livia Maria Della Porta Cosac, Cecilia Sevalho Goncalves, Marlei Josiele Augusto, Fernando Silva Ramalho, et al. (2017). Effect of Gallic Acid on Regression of Murine CCL4-Induced Hepatic Cirrhosis. International Journal of Homeopathy & Natural Medicines, 2(1), 15-19. https://doi.org/10.11648/j.ijhnm.20160201.13

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    ACS Style

    Sérgio Souza Figueiredo; Livia Maria Della Porta Cosac; Cecilia Sevalho Goncalves; Marlei Josiele Augusto; Fernando Silva Ramalho, et al. Effect of Gallic Acid on Regression of Murine CCL4-Induced Hepatic Cirrhosis. Int. J. Homeopathy Nat. Med. 2017, 2(1), 15-19. doi: 10.11648/j.ijhnm.20160201.13

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    AMA Style

    Sérgio Souza Figueiredo, Livia Maria Della Porta Cosac, Cecilia Sevalho Goncalves, Marlei Josiele Augusto, Fernando Silva Ramalho, et al. Effect of Gallic Acid on Regression of Murine CCL4-Induced Hepatic Cirrhosis. Int J Homeopathy Nat Med. 2017;2(1):15-19. doi: 10.11648/j.ijhnm.20160201.13

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  • @article{10.11648/j.ijhnm.20160201.13,
      author = {Sérgio Souza Figueiredo and Livia Maria Della Porta Cosac and Cecilia Sevalho Goncalves and Marlei Josiele Augusto and Fernando Silva Ramalho and Leandra Naira Zambelli Ramalho},
      title = {Effect of Gallic Acid on Regression of Murine CCL4-Induced Hepatic Cirrhosis},
      journal = {International Journal of Homeopathy & Natural Medicines},
      volume = {2},
      number = {1},
      pages = {15-19},
      doi = {10.11648/j.ijhnm.20160201.13},
      url = {https://doi.org/10.11648/j.ijhnm.20160201.13},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijhnm.20160201.13},
      abstract = {Hepatic cirrhosis can be induced by chronic exposure to reactive oxygen species (ROS). However, phenolic compounds, such as gallic acid (GA), appear to inhibit ROS-induced oxidative stress. We aimed to investigate the effects of GA on murine hepatic fibrogenesis. The effects of GA were evaluated on the regression of liver cirrhosis that was induced by chronic intraperitoneal CCl4 administration (20% v/v) in C57 mice for a period of 10 weeks. The animals were treated intraperitoneally and distributed in three groups, as follows: SHAM group – 8 weeks with Olive oil (CCL4 solution vehicle); C group – 8 weeks with CCL4 solution, and then 2 more weeks with deionized water (Gallic Acid solution vehicle); and C + GA group – 8 weeks with CCL4 solution, and then 2 more weeks with Gallic Acid solution (100 mg/Kg/day) on alternated days. The cirrhosis and inflammation-related factors were estimated using histological, western blotting and PCR-RT analysis. There was a significant decrease in the collagen deposition, as indicated by Sirius red staining, in the C + GA group compared to the C group (p<0.05). This improvement was accompanied by a reduction in the number of α-SMA-positive cells observed in these animals (p<0.05). The expression of the Procollagen α1(I), TGFβ1 and TIMP1 genes was also diminished by GA administration compared to the control (p<0.001). Additionally, proteomic studies revealed reduced p65 NFκB and p38 MAPK protein levels in the C + GA group. These findings reveal the effect of GA on the regression of cirrhosis. The mechanisms of this process might involve the anti-inflammatory activity of GA, which represses the TGFβ1, p65 NFκB, and p38 MAPK-mediated signaling pathways.},
     year = {2017}
    }
    

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  • TY  - JOUR
    T1  - Effect of Gallic Acid on Regression of Murine CCL4-Induced Hepatic Cirrhosis
    AU  - Sérgio Souza Figueiredo
    AU  - Livia Maria Della Porta Cosac
    AU  - Cecilia Sevalho Goncalves
    AU  - Marlei Josiele Augusto
    AU  - Fernando Silva Ramalho
    AU  - Leandra Naira Zambelli Ramalho
    Y1  - 2017/01/15
    PY  - 2017
    N1  - https://doi.org/10.11648/j.ijhnm.20160201.13
    DO  - 10.11648/j.ijhnm.20160201.13
    T2  - International Journal of Homeopathy & Natural Medicines
    JF  - International Journal of Homeopathy & Natural Medicines
    JO  - International Journal of Homeopathy & Natural Medicines
    SP  - 15
    EP  - 19
    PB  - Science Publishing Group
    SN  - 2472-2316
    UR  - https://doi.org/10.11648/j.ijhnm.20160201.13
    AB  - Hepatic cirrhosis can be induced by chronic exposure to reactive oxygen species (ROS). However, phenolic compounds, such as gallic acid (GA), appear to inhibit ROS-induced oxidative stress. We aimed to investigate the effects of GA on murine hepatic fibrogenesis. The effects of GA were evaluated on the regression of liver cirrhosis that was induced by chronic intraperitoneal CCl4 administration (20% v/v) in C57 mice for a period of 10 weeks. The animals were treated intraperitoneally and distributed in three groups, as follows: SHAM group – 8 weeks with Olive oil (CCL4 solution vehicle); C group – 8 weeks with CCL4 solution, and then 2 more weeks with deionized water (Gallic Acid solution vehicle); and C + GA group – 8 weeks with CCL4 solution, and then 2 more weeks with Gallic Acid solution (100 mg/Kg/day) on alternated days. The cirrhosis and inflammation-related factors were estimated using histological, western blotting and PCR-RT analysis. There was a significant decrease in the collagen deposition, as indicated by Sirius red staining, in the C + GA group compared to the C group (p<0.05). This improvement was accompanied by a reduction in the number of α-SMA-positive cells observed in these animals (p<0.05). The expression of the Procollagen α1(I), TGFβ1 and TIMP1 genes was also diminished by GA administration compared to the control (p<0.001). Additionally, proteomic studies revealed reduced p65 NFκB and p38 MAPK protein levels in the C + GA group. These findings reveal the effect of GA on the regression of cirrhosis. The mechanisms of this process might involve the anti-inflammatory activity of GA, which represses the TGFβ1, p65 NFκB, and p38 MAPK-mediated signaling pathways.
    VL  - 2
    IS  - 1
    ER  - 

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Author Information
  • Department of Pathology and Legal Medicine of Faculty of Medicine of Ribeir?o Preto, University of S?o Paulo, Riber?o Preto, Brazil

  • Department of Pathology and Legal Medicine of Faculty of Medicine of Ribeir?o Preto, University of S?o Paulo, Riber?o Preto, Brazil

  • Department of Pathology and Legal Medicine of Faculty of Medicine of Ribeir?o Preto, University of S?o Paulo, Riber?o Preto, Brazil

  • Department of Pathology and Legal Medicine of Faculty of Medicine of Ribeir?o Preto, University of S?o Paulo, Riber?o Preto, Brazil

  • Department of Pathology and Legal Medicine of Faculty of Medicine of Ribeir?o Preto, University of S?o Paulo, Riber?o Preto, Brazil

  • Department of Pathology and Legal Medicine of Faculty of Medicine of Ribeir?o Preto, University of S?o Paulo, Riber?o Preto, Brazil

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