INTRODUCTION: Enteral nutrition improves clinical outcomes. The effects of feeding on LPS induced liver injury are unknown. We hypothesized that feeding would attenuate liver injury from LPS. METHODS: Fasted or fed rats were given LPS (20 mg/kg i.p.) or saline for 5 h and sacrificed. Serum aminotransferases and cytokines (immunoassay) were measured. Oxidative stress protein (iNOS, COX2, and HO1) assessments (Western immunoblot) were also obtained. RESULTS: In fasted rats, LPS significantly increased serum aminotransferase levels, enhanced hepatic COX2, iNOS, and HO1 immunoreactivity, and increased serum cytokine levels when compared to controls. While feeding diminished liver enzymes, attenuated expression of COX2 and iNOS, and blunted production of pro-inflammatory cytokines, it did not modulate LPS-induced expression of the anti-inflammatory markers HO1 and IL-10. CONCLUSION: These data suggest that feeding decreases liver injury by attenuating expression of pro-inflammatory mediators while maintaining expression of anti-inflammatory mediators, both systemically and locally.
INTRODUCTION: Enteral nutrition improves clinical outcomes. The effects of feeding on LPS induced liver injury are unknown. We hypothesized that feeding would attenuate liver injury from LPS. METHODS: Fasted or fed rats were given LPS (20 mg/kg i.p.) or saline for 5 h and sacrificed. Serum aminotransferases and cytokines (immunoassay) were measured. Oxidative stress protein (iNOS, COX2, and HO1) assessments (Western immunoblot) were also obtained. RESULTS: In fasted rats, LPS significantly increased serum aminotransferase levels, enhanced hepatic COX2, iNOS, and HO1 immunoreactivity, and increased serum cytokine levels when compared to controls. While feeding diminished liver enzymes, attenuated expression of COX2 and iNOS, and blunted production of pro-inflammatory cytokines, it did not modulate LPS-induced expression of the anti-inflammatory markers HO1 and IL-10. CONCLUSION: These data suggest that feeding decreases liver injury by attenuating expression of pro-inflammatory mediators while maintaining expression of anti-inflammatory mediators, both systemically and locally.