Park Woo-Jae, Oh Eunyoung, Kim Yookyung
Department of Biochemistry, Chung-Ang University College of Medicine, Seoul 06974, Korea.
Interdisciplinary Program in Sustainable Living System, Graduate School, Korea University, Seoul 02841, Korea.
Nutr Res Pract. 2024 Oct;18(5):602-616. doi: 10.4162/nrp.2024.18.5.602. Epub 2024 Jun 11.
BACKGROUND/OBJECTIVES: Inflammation and ferroptosis are implicated in various diseases and lipopolysaccharides (LPS) have been linked with these disorders. Recently, many edible insects, such as larvae (PB) and larvae, have been recommended as alternative foods because they contain lots of nutritional sources. In this study, we explored the potential of PB extract in preventing LPS-induced inflammation and ferroptosis in Hep3B cells.
MATERIALS/METHODS: PB powder was extracted using 70% ethanol and applied to Hep3B cells. Co-treatment with LPS was conducted to induce ferroptosis and inflammation. The anti-inflammatory and anti-ferroptosis mechanisms of the PB extract were confirmed using Western blot, enzyme-linked immunosorbent assay, and real-time polymerase chain reaction analysis.
PB extract effectively prevented LPS-induced cell death and restored LPS-induced inflammatory cytokine production, NF-κB signaling, endoplasmic reticulum (ER) stress and ferroptosis. Interestingly, PB extract reduced LPS-induced ceramide increase and acid sphingomyelinase (ASMase) expression. The use of the ASMase inhibitor, desipramine, also demonstrated a reduction in these pathways, highlighting the pivotal role of ASMase in inflammation and ferroptosis. Treatment with each inhibitor revealed that ferroptosis causes ER stress and that NF-κB and MAP kinase pathways are involved in inflammation.
PB emerges as a potential functional food with inhibitory effects on LPS-induced inflammation and ferroptosis, making it a promising candidate for nutritional interventions.
背景/目的：炎症和铁死亡与多种疾病有关，脂多糖（LPS）与这些疾病相关。最近，许多食用昆虫，如 幼虫（PB）和 幼虫，因其含有大量营养成分而被推荐为替代食物。在本研究中，我们探讨了PB提取物在预防LPS诱导的Hep3B细胞炎症和铁死亡方面的潜力。
材料/方法：用70%乙醇提取PB粉末并应用于Hep3B细胞。与LPS共同处理以诱导铁死亡和炎症。使用蛋白质印迹法、酶联免疫吸附测定法和实时聚合酶链反应分析来确认PB提取物的抗炎和抗铁死亡机制。
PB提取物有效预防了LPS诱导的细胞死亡，并恢复了LPS诱导的炎性细胞因子产生、NF-κB信号传导、内质网（ER）应激和铁死亡。有趣的是，PB提取物减少了LPS诱导的神经酰胺增加和酸性鞘磷脂酶（ASMase）表达。使用ASMase抑制剂地昔帕明也显示这些途径减少，突出了ASMase在炎症和铁死亡中的关键作用。用每种抑制剂处理表明铁死亡导致ER应激，并且NF-κB和丝裂原活化蛋白激酶途径参与炎症。
PB作为一种潜在的功能性食品出现，对LPS诱导的炎症和铁死亡具有抑制作用，使其成为营养干预的有希望的候选者。
