Jamornwan Sopana, Chokpanuwat Tanida, Uppakara Kwanchanok, Soodvilai Sunhapas, Saengsawang Witchuda
Department of Physiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.
Chakri Naruebodindra Medical Institute, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Samut Prakan 10540, Thailand.
Biomedicines. 2022 Oct 15;10(10):2587. doi: 10.3390/biomedicines10102587.
Uncontrolled and excessive microglial activation is known to contribute to inflammation-mediated neurodegeneration. Therefore, reducing neurotoxic microglial activation may serve as a new approach to preventing neurodegeneration. Here, we investigated the anti-inflammatory effects of panduratin A against microglial activation induced by lipopolysaccharides (LPS) in the SIMA9 microglial cell line. We initially examined the anti-inflammatory properties of panduratin A by measuring LPS-induced nitric oxide (NO) production and the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). Panduratin A significantly reduced NO levels and pro-inflammatory cytokines' production and secretion. In addition, panduratin A enhanced the production of anti-inflammatory cytokines IL-4 and IL-10. The anti-inflammatory effects of panduratin A are related to the suppression of the NF-κB signaling pathway. Together, these results demonstrate the anti-inflammatory properties of panduratin A against LPS-induced microglial activation, suggesting panduratin A has the potential to be further developed as a new agent for the prevention of neuroinflammation-associated neurodegenerative diseases.
已知小胶质细胞的不受控制和过度激活会导致炎症介导的神经退行性变。因此，减少具有神经毒性的小胶质细胞激活可能成为预防神经退行性变的一种新方法。在此，我们研究了潘多拉丁A对脂多糖（LPS）诱导的SIMA9小胶质细胞系小胶质细胞激活的抗炎作用。我们首先通过测量LPS诱导的一氧化氮（NO）生成以及促炎细胞因子（TNF-α、IL-1β和IL-6）的水平来检测潘多拉丁A的抗炎特性。潘多拉丁A显著降低了NO水平以及促炎细胞因子的生成和分泌。此外，潘多拉丁A增强了抗炎细胞因子IL-4和IL-10的生成。潘多拉丁A的抗炎作用与抑制NF-κB信号通路有关。总之，这些结果证明了潘多拉丁A对LPS诱导的小胶质细胞激活具有抗炎特性，表明潘多拉丁A有潜力进一步开发成为预防神经炎症相关神经退行性疾病的新型药物。
