Gao Yuan, Chen Yanmei, Wang Ning, Meng Qiang
Department of Neurology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, China.
Medical School, Kunming University of Science and Technology, Kunming, Yunnan, China.
Immunopharmacol Immunotoxicol. 2025 Apr;47(2):201-212. doi: 10.1080/08923973.2025.2457960. Epub 2025 Feb 9.
Albiflorin isolated from can cross the blood-brain barrier (BBB) and possesses analgesia, anticonvulsant, anti-inflammatory, and hepatoprotective properties. This study investigates albiflorin functions and related mechanisms in Parkinson's disease (PD) pathogenesis.
Cellular and animal models of PD were constructed. Cell viability and apoptosis were detected by CCK-8 assays. Levels of Iba-1 and TH were measured by immunofluorescence staining, western blotting, and immunohistochemistry staining. Levels of pro-inflammatory mediators and pathway-related genes were measured by western blotting and RT-qPCR. Locomotor activity of mice was examined by open field test, rod climbing test, and rod rotating test.
For analysis, albiflorin inhibited LPS-induced microglial activation and neuroinflammation. Additionally, albiflorin inactivated NF-κB and MAPK pathways in LPS-treated BV2 cells. Moreover, albiflorin attenuated neurotoxicity mediated by LPS-stimulated microglia. For analysis, albiflorin improved MPTP-induced locomotor activity deficits and reduced MPTP-induced dopaminergic neuron loss. In parallel, albiflorin inhibited activated microglia-mediated neuroinflammation in MPTP-treated mice.
Albiflorin mitigates neuronal apoptosis and improves behavioral impairments in MPTP-induced PD mouse model through inhibition of activated microglia-mediated neuroinflammation the NF-κB and MAPK pathways.
从[具体来源未提及]分离出的白花芍药苷能够穿过血脑屏障（BBB），并具有镇痛、抗惊厥、抗炎和肝保护特性。本研究探讨白花芍药苷在帕金森病（PD）发病机制中的作用及相关机制。
构建PD细胞模型和动物模型。采用CCK-8法检测细胞活力和凋亡情况。通过免疫荧光染色、蛋白质印迹法和免疫组织化学染色检测Iba-1和TH的水平。采用蛋白质印迹法和RT-qPCR检测促炎介质和通路相关基因的水平。通过旷场试验、杆攀爬试验和杆旋转试验检测小鼠的运动活性。
在[此处未明确具体实验名称，推测与前文对应]分析中，白花芍药苷抑制脂多糖（LPS）诱导的小胶质细胞活化和神经炎症。此外，白花芍药苷使LPS处理的BV2细胞中的核因子κB（NF-κB）和丝裂原活化蛋白激酶（MAPK）通路失活。而且，白花芍药苷减轻了LPS刺激的小胶质细胞介导的神经毒性。在[此处未明确具体实验名称，推测与前文对应]分析中，白花芍药苷改善了1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的运动活性缺陷，并减少了MPTP诱导的多巴胺能神经元损失。同时，白花芍药苷抑制了MPTP处理小鼠中活化的小胶质细胞介导的神经炎症。
白花芍药苷通过抑制活化的小胶质细胞介导的神经炎症以及NF-κB和MAPK通路，减轻MPTP诱导的PD小鼠模型中的神经元凋亡并改善行为障碍。
