Abstract
Liver fibrosis is a wound-healing response to chronic liver injury characterized by progressive inflammation and deposition of extracellular matrix components. The pathological condition of liver fibrosis involves secretion of extracellular matrix proteins and formation of scar tissue. The major regulators involved in hepatic fibrogenesis are the transforming growth factor (TGF)-β1/SMAD and toll-like receptor 4 (TLR4)-initiated myeloid differentiation primary response 88 gene (MyD88)/NF-ĸB cell signaling pathways. This article reviews natural products and herbal medicines that have demonstrated activity against liver fibrosis through different mechanisms of action, including anti-hepatitis B and C virus activity, anti-inflammation, inhibition of cytokine production and nuclear receptor activation, and free radical scavenging.
Highlights
Chronic liver injury increases extracellular matrix (ECM) deposition by activating the hepatic stellate cells (HSCs). This results in liver fibrosis, which is a major cause of mortality worldwide mainly because of chronic infection with the hepatitis virus and obesity associated with fatty liver disease [1]
Cirrhosis occurs in the final stage of liver fibrosis and is characterized by the distortion of liver vasculature and architecture that increases the likelihood of liver failure and primary liver cancer [2]
We review natural products and herbal medicines that have demonstrated activity against liver fibrosis through different mechanisms of action, including anti-hepatitis B and C virus activity, anti-inflammation, inhibition of cytokine production and nuclear receptor activation, and free radical scavenging
Summary
Chronic liver injury increases extracellular matrix (ECM) deposition by activating the hepatic stellate cells (HSCs). NF-κB will be released from the IκB kinase complex and translocate into the nucleus after IκBα phosphorylated and ubiquitinated [18], inducing transcription of inflammatory cytokines related to liver fibrogenesis, including interleukin 6 (IL-6), IL-12, and tumor necrosis factor α (TNFα) [19]. The activated HSCs in the fibrotic liver undergo an EMT as revealed by elevated mesenchymal and epithelial markers [35] Other regulators, such as cadherins, microRNAs, transcription factors (e.g., Pax, paraxis, and Fox) and growth factors (e.g., Wnts, FGFs, and ephrins) are involved in maintaining the balance of EMT and MET [36,37].
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