The aim of this study was to investigate the anti-inflammatory properties of Pandanus conoideus Lamk (red fruit oil [RFO]) and establish the signal pathway of the leading compounds. RAW 264.7 murine macrophage cells were used with lipopolysaccharide (LPS). Cell viability and the pro-inflammatory factors were investigated using MTT assay, real-time polymerase chain reaction (PCR), western blot analysis, and enzyme-linked immunosorbent assay. The quantification of leading compounds in RFO was performed using high-performance liquid chromatography (HPLC). RFO did not reduce RAW 264.7 cell viability. RFO significantly reduced the production of nitric oxide (NO), cyclooxygenase-2, and prostaglandin E₂, and both the protein level and mRNA level of inducible NO synthase in LPS-induced macrophages. RFO also regulated the reactive oxygen species (ROS) in LPS-induced macrophages. RFO attenuated the translocation of the nuclear factor κB (NF-κB) p65 subunit, phosphorylation of I-κB, p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase (JNK) in a dose-dependent manner. HPLC analysis determined that 1 g of RFO had 14.05 ± 0.8 mg of β-cryptoxanthin and 7.4 ± 0.7 mg of β-carotene. In conclusion, RFO provides an anti-inflammatory effect by regulating ROS and NF-κB through mitogen-activated protein kinase due to antioxidant activity.

这项研究的目的是研究露兜树（Padanus conoideus Lamk）（红色果油[RFO]）的抗炎特性，并建立主要化合物的信号通路。RAW 264.7鼠巨噬细胞与脂多糖（LPS）一起使用。使用MTT分析，实时聚合酶链反应（PCR），western印迹分析和酶联免疫吸附试验研究细胞活力和促炎因子。使用高效液相色谱（HPLC）对RFO中的主要化合物进行定量。RFO没有降低RAW 264.7细胞的活力。RFO显着减少了一氧化氮（NO），环氧合酶2和前列腺素E _2的产生，以及LPS诱导的巨噬细胞中诱导型NO合酶的蛋白水平和mRNA水平。RFO还调节LPS诱导的巨噬细胞中的活性氧（ROS）。RFO以剂量依赖的方式减弱了核因子κB（NF-κB）p65亚基的易位，I-κB，p38，细胞外信号调节激酶和c-Jun N末端激酶（JNK）的磷酸化。HPLC分析确定1g RFO具有14.05±0.8mg的β-隐黄质和7.4±0.7mg的β-胡萝卜素。总之，由于抗氧化活性，RFO通过有丝分裂原激活的蛋白激酶调节ROS和NF-κB，从而提供抗炎作用。