Panaxynol (PAL) mainly comes from Umbelliferae plants, which has anti-inflammatory and neuroprotective activities. Lipopolysaccharide (LPS)-induced depression in mice was a classic model for studying the effects of drugs on depression in mice. The purpose of this study was to investigate the mechanism and effect of PAL on depression by LPS induced in mice. In the tail suspension test (TST) and forced swimming test (FST) results, PAL significantly reduced the immobility time of mice. In the result of the open field test (OFT) and the elevated plus maze test (EPM), improved their exploration ability. According to the results of ELISA, PAL could significantly reduce the tumor necrosis factor-α (TNF-α) and interleukin- 6 (IL-6) levels in serum. Increase the superoxide dismutase (SDO) level and decrease the malondialdehyde (MDA) level in hippocampus. According to Western blotting analysis results, PAL increased the protein expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB), decreased the nuclear transport of nuclear factor kappa-Bp65 (NF-κBp65) and phosphorylation of inhibitor of NF-κB (IκB-α). Meanwhile, PAL also inhibited the production of nitric oxide in BV-2 microglia and decreased the level of inflammatory factors. PAL also reduced levels of oxidative stress and inhibited protein expression in the NF-κB/IκB-α inflammatory pathway and increased the protein expression of BDNF/TrkB, thereby inhibiting the over-activation of BV-2 microglia. In conclusion, according to the results of the behavioral text, it is proved that PAL could effectively alleviate LPS induced depression behavior in mice. The mechanism may be that the anti-inflammatory and anti-oxidative stress effects of PAL reduce the release of inflammatory factors in the mouse brain. Meanwhile, PAL could improve brain neurotrophic factors, inhibit the excessive activation of BV-2 microglia, and further inhibit the depressive state of the mice.

人参三醇（PAL）主要来自伞形科植物，具有抗炎和神经保护作用。脂多糖（LPS）引起的小鼠抑郁是研究药物对小鼠抑郁影响的经典模型。这项研究的目的是研究PAL抑制LPS诱导的小鼠抑郁的机制和作用。在尾部悬架测试（TST）和强迫游泳测试（FST）的结果中，PAL显着减少了小鼠的固定时间。通过野外测试（OFT）和高架迷宫测试（EPM）的结果，提高了其勘探能力。根据ELISA结果，PAL可以显着降低血清中的肿瘤坏死因子-α（TNF-α）和白细胞介素6（IL-6）水平。增加海马中的超氧化物歧化酶（SDO）水平并降低丙二醛（MDA）水平。根据Western印迹分析结果，PAL可增加脑源性神经营养因子（BDNF）和酪氨酸激酶受体B（TrkB）的蛋白表达，降低核因子kappa-Bp65（NF-κBp65）的核转运，并抑制PAL的磷酸化。 NF-κB（IκB-α）。同时，PAL还抑制了BV-2小胶质细胞中一氧化氮的产生，并降低了炎症因子的水平。PAL还降低了氧化应激水平，并抑制了NF-κB/IκB-α炎症途径中的蛋白质表达，并增加了BDNF / TrkB的蛋白质表达，从而抑制了BV-2小胶质细胞的过度活化。总之，根据行为文本的结果，证明了PAL可以有效减轻LPS诱导的小鼠抑郁行为。其机制可能是PAL的抗炎和抗氧化应激作用减少了小鼠大脑中炎性因子的释放。同时，PAL可以改善脑神经营养因子，抑制BV-2小胶质细胞的过度活化，并进一步抑制小鼠的抑郁状态。