Figure 2.

Proposed mechanisms involved in the anti-fibrotic activity of curcumin by inhibiting the activation of PSCs to acquire myofibroblast-like phenotypes. Curcumin attenuates the production of TNF-α-induced MCP-1. Besides, it can also significantly reduce the activation of MAPKs signaling, such as c-Jun N-terminal kinase (JNK), P38 MAPK and ERK, which are pivotal in stimulating the production of inflammatory cytokines and mediators. Additionally, curcumin further down-regulates NF-κB signaling pathway by reducing its subunit P65. Apart from these, curcumin can notably reduce the gene expression of α-SMA, IL-1β, Col I and Col III as well as diminish PSCs activation by downregulating the mRNA expression levels of several fibrogenic mediators, including Acta 2, Col-α1 and FN1, under the stimulating effects of TGF-β.