Cheng Binfeng, Dong Yuqian, Li Xiaolu, Yu Haoheng, Feng Yu, Wang Yilong, Liu Yaxin, Liu Chen, Wang Lei
Xinxiang Key Laboratory of Cellular Stress Biology, School of Life Sciences and Technology; The Third Affiliated Hospital, Xinxiang Medical University, Xinxiang, Henan.
Xinxiang Key Laboratory of Cellular Stress Biology, School of Life Sciences and Technology.
Pharmazie. 2025 Aug 1;80(4):55-59. doi: 10.1691/ph.2025.5532.
Activation of microglia plays a pivotal role in the pathogenesis of neuroinflammation-mediated neurodegenerative diseases. Glycyrrhizic acid (GA), a principal triterpenoid saponin in , has been reported to exhibit a range of biological activities. Nevertheless, the function of GA in microglia activation remains unclear. In this study, the effects and mechanisms of GA on the inflammatory response were investigated in the lipopolysaccharides (LPS)-stimulated microglial BV2 cells. BV2 cells were treated with GA (0, 20 and 50 μM), followed by stimulation with LPS (1 μg/mL). The results demonstrated that GA significantly inhibited the expression of tumor necrosis factor-α (TNF-α ) and interleukin-1β (IL-1β) at the mRNA and protein levels induced by LPS. Furthermore, the release of reactive oxygen species (ROS) and the migration of microglia were suppressed by GA in LPS-stimulated BV2 cells. In addition, GA reduced the activation of mitogen-activated protein kinases (MAPKs) and the phosphorylation of Akt. GA also inhibited the phosphorylation of Iκ Bα kinase (IKK) and p65, and blocked the nuclear translocation of p65 protein. The findings indicate that GA inhibited the inflammatory response in LPS-stimulated microglial BV2 cells through the suppression of MAPK, Akt, and nuclear factor-κ B (NF-κ B) signaling pathways, suggesting that GA may serve as a potential therapeutic approach for the treatment of neuroinflammation-associated neurodegenerative diseases.
小胶质细胞的激活在神经炎症介导的神经退行性疾病发病机制中起关键作用。甘草酸（GA）是甘草中的一种主要三萜皂苷，据报道具有一系列生物学活性。然而，GA在小胶质细胞激活中的作用仍不清楚。在本研究中，研究了GA对脂多糖（LPS）刺激的小胶质细胞BV2细胞炎症反应的影响及其机制。用GA（0、20和50μM）处理BV2细胞，然后用LPS（1μg/mL）刺激。结果表明，GA在mRNA和蛋白水平上显著抑制LPS诱导的肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的表达。此外，GA抑制了LPS刺激的BV2细胞中活性氧（ROS）的释放和小胶质细胞的迁移。此外，GA降低了丝裂原活化蛋白激酶（MAPKs）的激活和Akt的磷酸化。GA还抑制了IκBα激酶（IKK）和p65的磷酸化，并阻断了p65蛋白的核转位。这些发现表明，GA通过抑制MAPK、Akt和核因子-κB（NF-κB）信号通路来抑制LPS刺激的小胶质细胞BV2细胞中的炎症反应，提示GA可能作为治疗神经炎症相关神经退行性疾病的一种潜在治疗方法。
