Copper Mediates Anti-Inflammatory and Antifibrotic Activity of Gleevec in Hepatocellular Carcinoma-Induced Male Rats

Figure 7

A suggested diagram showing the possible mechanism of the fibrosis stage observed in the liver tissue. The carcinogen-induced hepatic inflammation post-secretion of immunomediators can trigger fibrogenesis by inducing programmed cell death in the hepatocytes, while apoptotic bodies TGFβ1, PDGF, EGF, etc. can activate nascent hepatic stellate cells transforming them into myofibroblasts. On the other hand, Cu mediates the downregulation of NF-κB and TNF-α and growth factors leading to the suppression of the inflammatory cascade and suppression of stellate cells in the treated rats.