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      Drug Design, Development and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the design and development of drugs, as well as the clinical outcomes, patient safety, and programs targeted at the effective and safe use of medicines. Sign up for email alerts here.

      88,007 Monthly downloads/views I 4.319 Impact Factor I 6.6 CiteScore I 1.12 Source Normalized Impact per Paper (SNIP) I 0.784 Scimago Journal & Country Rank (SJR)

       

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      Ginkgo biloba extract mitigates liver fibrosis and apoptosis by regulating p38 MAPK, NF-κB/IκBα, and Bcl-2/Bax signaling.

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          Abstract

          Liver fibrosis is the consequence of diverse liver injuries and can eventually develop into liver cirrhosis. Ginkgo biloba extract (GBE) is an extract from dried ginkgo leaves that has many pharmacological effects because of its various ingredients and has been shown to be hepatoprotective.

          Most cited references48

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          Hepatic fibrosis -- overview.

          Katherine Friedman (2008)
          The study of hepatic fibrosis, or scarring in response to chronic liver injury, has witnessed tremendous progress in the past two decades. Clarification of the cellular sources of scar, and emergence of hepatic stellate cells not only as a fibrogenic cell type, but also as a critical immunomodulatory and homeostatic regulator are among the most salient advances. Activation of hepatic stellate cells remains a central event in fibrosis, complemented by evidence of additional sources of matrix-producing cells including bone marrow, portal fibroblasts, and epithelial-mesenchymal transition from both hepatocytes and cholangiocytes. A growing range of cytokines and their receptors and inflammatory cell subsets have further expanded our knowledge about this dynamic process. Collectively, these findings have laid the foundation for continued elucidation of underlying mechanisms, and more importantly for the implementation of rationally based approaches to limit fibrosis, accelerate repair and enhance liver regeneration in patients with chronic liver disease.
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            Aberrantly expressed Fra-1 by IL-6/STAT3 transactivation promotes colorectal cancer aggressiveness through epithelial–mesenchymal transition

            Hong-Hong Liu, Guoping Ren, Tingyang Wang … (2015)
            Summary This study describes a novel mechanism of the inflammatory cytokine IL-6 induced Fra-1 upregulation through activating STAT3 by phosphorylation and acetylation, and demonstrates that this signaling pathway plays a critical role in promoting epithelial–mesenchymal transition and aggressiveness of colorectal cancer.
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              Liver fibrosis: cellular mechanisms of progression and resolution.

              Neil C Henderson, John P Iredale (2007)
              Liver fibrosis represents a major worldwide health care burden. The last 15 years have seen a rapid growth in our understanding of the pathogenesis of this clinically relevant model of inflammation and repair. This work is likely to inform the design of effective antifibrotic therapies in the near future. In this review, we examine how the innate and adaptive immune response interacts with other key cell types in the liver, such as the myofibroblast, regulating the process of hepatic fibrosis and, where relevant, resolution of fibrosis with remodelling. Emphasis is placed on the increasing knowledge that has been generated by the use of transgenic animals and animals in which specific cell lines have been deleted. Additionally, we review the increasing evidence that, although significant numbers of wound-healing myofibroblasts are derived from the hepatic stellate cell, significant contributions may occur from other cell lineages, including those from distant sites such as bone marrow stem cells.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Drug Des Devel Ther
                Title: Drug design, development and therapy
                Publisher: Informa UK Limited
                ISSN (Electronic): 1177-8881
                ISSN (Print): 1177-8881
                Publication date (Electronic): 2015
                Volume: 9
                Affiliations
                [1 ] Department of Pharmacy, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
                Article
                Publisher Item ID: dddt-9-6303
                DOI: 10.2147/DDDT.S93732
                PMC ID: 4671772
                PubMed ID: 26664050
                SO-VID: 149514c4-108a-403b-8ffc-92de52724a93
                History

                Keywords: hepatoprotective,rats,mechanism,HSCs activation,inflammation,pathways
                Data availability:
                Keywords: hepatoprotective, rats, mechanism, HSCs activation, inflammation, pathways

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