Acute Inflammation and Oxidative Stress Induced by Lipopolysaccharide and the Ameliorative Effect of Stingless Bee Honey

Background: Systemic acute inflammation is the hallmark of sepsis and is associated with multiple organ dysfunction. Objective: This study investigated the potential of Stingless Bee Honey (SBH) to suppress lipopolysaccharide (LPS)-induced systemic acute inflammation in rats and to reveal the probable mechanism of action. Methods: Rats received 4.6 and 9.2 g/kg SBH for 7 days followed by a single injection of LPS after which blood samples were taken 6h later. Results: LPS induced liver, kidney, heart, and lung injury, were manifested by increased serum transaminases, alkaline phosphatase, creatine kinase, creatinine, and urea, along with multiple histological alterations, particularly leukocyte infiltration. Pro-inflammatory cytokines were elevated in the serum, and NF-kappa B p65, p38 MAPK, and HMGB-1 were significantly increased in different tissues of LPS-challenged rats. SBH prevented tissue injury, ameliorated pro-inflammatory cytokines, and suppressed NF-kappa B p65, p38 MAPK, and HMGB-1 in rats that had received LPS. In addition, SBH diminished reactive oxygen species (ROS) production, lipid peroxidation, and oxidative DNA damage, and enhanced glutathione and Nrf2 in LPS-treated rats. Conclusion: SBH prevents systemic acute inflammation by suppressing NF-kappa B, p38 MAPK, HMGB-1, oxidative stress, and tissue injury in rats. Thus, SBH may represent an effective anti-inflammatory nutraceutical, pending further mechanistic studies.

Automated summary

The study demonstrated the potential of Stingless Bee Honey in suppressing systemic acute inflammation induced by lipopolysaccharide in rats. It works by preventing tissue injury, ameliorating pro-inflammatory cytokines, and reducing oxidative stress. This suggests that Stingless Bee Honey may be an effective anti-inflammatory nutraceutical deserving further mechanistic studies.