Published online Oct 21, 2014. doi: 10.3748/wjg.v20.i39.14430
Revised: March 6, 2014
Accepted: June 2, 2014
Published online: October 21, 2014
Processing time: 284 Days and 7.9 Hours
AIM: To examine the effect of farnesoid X receptor (FXR) activation by GW4064 on endotoxin-induced hepatic inflammation in nonalcoholic fatty liver disease (NAFLD) and the underlying mechanism.
METHODS: Six-week-old male C57BL/6 mice were fed a normal diet or a high-fat (HF) diet for 8 wk. HF diet-fed mice were intraperitoneally injected with GW4064 (30 mg/kg) or DMSO (vehicle) once daily for a week and then sacrificed after lipopolysaccharide (LPS, 50 μg/mouse) administration. Hepatic inflammation, levels of the macrophage marker F4/80, and apoptosis were measured at the end of the study. Additionally, the expression of proinflammatory genes involved in NAFLD (interleukin-6, interleukin-1β, interferon-γ, MCP-1) were analyzed by real-time PCR in the murine macrophage cell line RAW 264.7 cultured with or without GW4064 (2 μmol/L) before treatment with LPS.
RESULTS: In patients with NAFLD, the expression of FXR was detected by immunohistochemical staining and the relation between FXR expression and NAFLD activity score (NAS) was analyzed. Activation of FXR by GW4064 alleviated hepatic inflammation induced by endotoxin in a murine NAFLD model fed an HF diet as reflected by reduced serum levels of aspartate aminotransferase and alanine aminotransferase. Apoptosis and proinflammatory cytokine levels in liver tissues were also reduced by GW4064, and GW4064 could reduce induction of proinflammatory cytokines by LPS in vitro. FXR levels were reduced in patients with non-alcoholic steatohepatitis compared with healthy controls and were negatively correlated with NAS.
CONCLUSION: FXR activation attenuates LPS-induced hepatic inflammation in murine NAFLD by reducing expression of proinflammatory cytokines in macrophages.
Core tip: We found that the synthetic farnesoid X receptor (FXR) agonist GW4064 attenuated lipopolysaccharide-induced hepatic injury in high-fat diet-fed mice by reducing proinflammatory cytokine expression in macrophages. Moreover, we found that FXR expression was decreased in patients with nonalcoholic steatohepatitis, the most extreme form of nonalcoholic fatty liver disease (NAFLD), and was inversely correlated with the NAFLD activity score. Together, these findings provide insights into the etiology of NAFLD and suggest that FXR activation with synthetic agonists may represent a potential therapeutic option for patients with NAFLD, which we believe will be of great interest to the readers of the journal.