Interestingly, hepatocytes from ethanol-fed RXR null mice show an increased NF-kB activation and a strong and higher induction of inflammatory cytokines TNF-α, IL-1 and IL-6, compared to wild-type mice [107]. Apoptosis in RXR null mice increases after ethanol ingestion due to a lower expression of antiapoptotic proteins Bcl2 and Bcl-XL, even in the presence of higher levels of IL-6. RXR seems to influence IL-6/STAT3 mediated signalling circumventing STAT3 phosphorylation [107]. This suggests that RXR is an important regulator of inflammatory processes in response to ethanol; it may also be speculated that some of the effects in response to LPS (as describer above) may be ascribed to RXR reduced expression.
