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-κB 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-κB 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-κB, p38 MAPK, HMGB-1, oxidative stress, and tissue injury in rats. Thus, SBH may represent an effective anti-inflammatory nutraceutical, pending further mechanistic studies.

背景：全身性急性炎症是败血症的标志，并与多器官功能障碍有关。

目的：本研究调查了无刺蜜蜂蜂蜜 (SBH) 抑制脂多糖 (LPS) 诱导的大鼠全身性急性炎症的潜力，并揭示可能的作用机制。

方法：大鼠接受 4.6 和 9.2 g/kg SBH 7 天，然后单次注射 LPS，6 小时后采集血样。

结果：LPS 诱导的肝、肾、心和肺损伤表现为血清转氨酶、碱性磷酸酶、肌酸激酶、肌酐和尿素增加，以及多种组织学改变，特别是白细胞浸润。血清促炎细胞因子升高，LPS攻击大鼠不同组织中NF-κB p65、p38 MAPK和HMGB-1显着升高。在接受 LPS 的大鼠中，SBH 可防止组织损伤、改善促炎细胞因子并抑制 NF-κB p65、p38 MAPK 和 HMGB-1。此外，SBH 减少了活性氧 (ROS) 的产生、脂质过氧化和 DNA 氧化损伤，并增强了 LPS 治疗大鼠的谷胱甘肽和 Nrf2。

结论：SBH 通过抑制大鼠 NF-κB、p38 MAPK、HMGB-1、氧化应激和组织损伤来预防全身性急性炎症。因此，SBH 可能代表一种有效的抗炎营养品，有待进一步的机制研究。