Abstract
During chronic liver injury, hepatic stellate cells (HSC) are activated and proliferate, which causes excessive extracellular matrix (ECM) deposition, leading to scar formation and fibrosis. Medicinal plants are gaining popularity as antifibrotic agents, and are often safe, cost-effective, and versatile. This review aims to describe the protective role and mechanisms of medicinal plants in the inhibition of HSC activation and ECM deposition during the pathogenesis of liver fibrosis. A systematic literature review on the anti-fibrotic mechanisms of hepatoprotective plants was performed in PubMed, which yielded articles about twelve relevant plants. Many of these plants act via disruption of the transforming growth factor beta 1 signaling pathway, possibly through reduction in oxidative stress. This reduction could explain the inhibition of HSC activation and reduction in ECM deposition. Medicinal plants could be a source of anti-liver fibrosis compounds.Electronic supplementary materialThe online version of this article (doi:10.1186/s13020-014-0027-4) contains supplementary material, which is available to authorized users.
Highlights
Liver fibrosis is caused by inappropriate tissue repair via connective tissue deposition, which results from chronic liver injuries, including those from alcohol, chronic viral hepatitis, autoimmune diseases, parasites, metabolic diseases, and toxins or other drugs [1]
Hundreds of thousands of people worldwide suffer from cirrhosis, partially because of the obesity pandemic combined with the high incidence of alcohol abuse and viral hepatitis [4]
This review aims to describe the role of some hepatoprotective plants in the inhibition of hepatic stellate cells (HSC) activation and extracellular matrix (ECM) deposition in the pathogenesis of liver fibrosis
Summary
Liver fibrosis is caused by inappropriate tissue repair via connective tissue deposition, which results from chronic liver injuries, including those from alcohol, chronic viral hepatitis, autoimmune diseases, parasites, metabolic diseases, and toxins or other drugs [1]. TGF-β1, produced by HSCs and other neighboring cell types like Kupffer cells, sinusoidal endothelial cells, bile duct epithelial cells, and hepatocytes [11], is a potent fibrogenic signal [20] as it increases the production of collagen I and other matrix constituents like fibronectin and proteoglycans [12,21] These effects are induced by the interaction between TGF-β1 and the membrane receptor complex formed by TβRI and TβRII, leading to the phosphorylation of intracellular mediators, namely Smad proteins. HSCs, neutrophils, and macrophages are the main cellular contributors to ECM degradation [1], while HSCs, portal myofibroblasts, bone-marrowderived cells, and the epithelial–mesenchymal transition are responsible for ECM synthesis [14] All these cells involve several molecular effectors such as matrix proteins, MMPs and TIMPs. During fibrogenesis, several ECM proteins, especially collagens type I, III, and IV; proteoglycans; laminin; and fibronectin are over-expressed by activated HSCs and other cells, which results in pathological scar formation [131]. Plant compound targets include multiple components of the ECM, such as collagen species, laminin, and fibronectin, as well as MMPs, TIMPs, and the plasminogen activation system (Table 2)
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