Wei Wei, Wu Jing, Zhang Dandan, Xu Shoucheng, Wang Yi, Li Xuezhong, Yu Ming, Chen Xiaopeng
Department of Neurology, The Affiliated People's Hospital of Jiangsu University, Zhenjiang Jiangsu, PR China.
Department of Neurology, Jurong Hospital Affiliated to Jiangsu University, Jurong, PR China.
Histol Histopathol. 2025 Sep;40(9):1457-1466. doi: 10.14670/HH-18-874. Epub 2025 Jan 16.
Parkinson's disease (PD) is a limb movement disorder caused by the degeneration of brain neurons and seriously affects the quality of life of the elderly. However, the current drugs are symptomatic treatments that cannot prevent or delay the development of the disease. Targeted therapy for pathogenesis may be the direction of development in the future. Oxidative stress and the inflammatory response are involved in the pathogenesis of PD. Edaravone and scutellarin have been studied in antioxidant and anti-inflammatory reactions. The focus of this study is whether there is synergy between the two and its mechanism. Through research, we found that edaravone and scutellarin at different dose combinations have synergistic effects in 1-methyl-4-phenylpyridinium (MPP+)-induced PC12 cells using the Chou-Talalay joint index method. According to the CompuSyn software calculation, the results showed that the combination index (CI) of the combined application of 15 µM edaravone and 15 µM scutellarin was the lowest, indicating that the synergistic effect was the best. Compared with the single drug, the synergy increased superoxide dismutase (SOD) and reduced glutathione (GSH) levels, reduced the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and enhanced the anti-apoptosis ability in the MPP(+) induced cell model of PD.
帕金森病（PD）是一种由脑神经元变性引起的肢体运动障碍，严重影响老年人的生活质量。然而，目前的药物都是对症治疗，无法预防或延缓疾病的发展。针对发病机制的靶向治疗可能是未来的发展方向。氧化应激和炎症反应参与了PD的发病机制。依达拉奉和灯盏花素已在抗氧化和抗炎反应方面进行了研究。本研究的重点是两者之间是否存在协同作用及其机制。通过研究，我们发现使用Chou-Talalay联合指数法，依达拉奉和灯盏花素在不同剂量组合下对1-甲基-4-苯基吡啶离子（MPP+）诱导的PC12细胞具有协同作用。根据CompuSyn软件计算，结果表明15μM依达拉奉和15μM灯盏花素联合应用的组合指数（CI）最低，表明协同作用最佳。与单一药物相比，协同作用提高了超氧化物歧化酶（SOD）和还原型谷胱甘肽（GSH）水平，降低了肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）水平，并增强了MPP（+）诱导的PD细胞模型中的抗凋亡能力。
