Kupffer cell depletion attenuates IL-6/STAT3 mediates hepatocyte apoptosis in immunological liver injury of trichloroethylene sensitized mice.

Abstract Trichloroethylene (TCE) induced TCE hypersensitivity syndrome which makes immune injuries in multi-system. The multiple organ damage included skin, liver, kidney and so on. The main manifestations of liver injuries were apoptosis and edema of hepatocytes. In our previous research, we found the activation of Kupffer cells (KCs) which increased IL-6 can aggravate liver cell apoptosis in TCE sensitized mice. However, the mechanism of IL-6 in liver damages induced by TCE was not clear. This study explored the function of IL-6/STAT3 signal pathway on the TCE induced apoptosis of liver cell. We established a TCE sensitized BALB/c mouse model with a KCs inhibitor GdCl3, we found that the expressions of ALT and AST in TCE sensitization positive mice were higher than other mice, and the expressions of apoptosis-related proteins were up-regulated in TCE sensitization positive mice, GdCl3 could alleviate this process. Meanwhile, GdCl3 could significantly decrease the expressions of IL-6/STAT3 proteins. All in all, the activation of KCs can increase the expression of IL-6, IL-6R and phosphorylate STAT3, induces hepatocyte apoptosis, and participates in immunity damage of liver which induced by TCE.