目的：探讨槲皮素（QUE）对帕金森病（PD）小鼠行为学障碍及核因子E2相关因子2-抗氧化反应元件（Nrf2-ARE）信号通路的影响。方法：将BALB/c小鼠随机分为对照组（Control组）、PD组、QUE低剂量组（QUE-L组）、高剂量组（QUE-H组）、QUE高剂量+通路抑制剂ML385组（QUE-H+ML385组），每组18只；给药结束，对BALB/c小鼠行为进行检测；酶联免疫吸附测定检测氧化应激[丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）]水平；HE染色观察脑组织黑质病理变化情况；尼氏染色观察神经元的存活情况；免疫组织化学法检测脑黑质区酪氨酸羟化酶（TH）、α-突触核蛋白（α-syn）表达情况；免疫印迹检测Nrf2-ARE信号通路相关蛋白表达情况。结果：PD组较Control组黑质多巴胺能神经元排列紊乱，神经元数量减少且细胞体皱缩，尼氏小体数量减少，小鼠悬挂实验评分降低，滚轴平衡时间减短，过平衡杆时间延长，MDA水平及α-syn表达升高，SOD、GSH-Px水平及TH、Nrf2、醌氧化还原酶（NQO1）表达降低（P＜0.05）；QUE-L、QUE-H组较PD组黑质多巴胺能神经元排列相对有序，神经元数量增多且形态相对正常，尼氏小体数量增多，小鼠悬挂实验评分升高，滚轴平衡时间延长，过平衡杆时间减短，MDA水平及α-syn表达降低，SOD、GSH-Px水平及TH、Nrf2、NQO1表达升高（P＜0.05）；QUE-H+ML385组较QUE-H组多巴胺能神经元排列紊乱，神经元数量减少明显且形态异常，尼氏小体数量减少明显，小鼠悬挂实验评分降低，滚轴平衡时间减短，过平衡杆时间延长，MDA水平及α-syn表达升高，SOD、GSH-Px水平及TH、Nrf2、NQO1表达降低（P＜0.05）。结论：QUE可改善PD小鼠运动行为障碍，可能与激活Nrf2-ARE信号通路有关。

Objective: To investigate the effects of quercetin (QUE) on behavioral disorders and the nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling pathway in Parkinson's disease (PD) mice. Methods: BALB/c mice were randomly divided into control group, PD group, low-dose QUE group (QUE-L group), high-dose QUE group (QUE-H group), and high-dose QUE combined with pathway inhibitor ML385 group (QUE-H+ML385 group), with 18 mice in each group. After drug administration, the behavioral performance of BALB/c mice was evaluated. Enzyme-linked immunosorbent assay was used to detect the levels of oxidative stress markers including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). Hematoxylin-eosin staining was applied to observe the pathological changes in the substantia nigra of brain tissue, and Nissl staining was used to assess the survival of neurons. Immunohistochemistry was performed to detect the expressions of tyrosine hydroxylase (TH) and α-synuclein (α-syn) in the substantia nigra region, and Western blot was used to measure the expressions of proteins related to the Nrf2-ARE signaling pathway. Results: Compared with the control group, the PD group showed disorganized arrangement of nigral dopaminergic neurons, reduced number of neurons with shrunken cell bodies, decreased number of Nissl bodies, lower suspension test scores, shorter rolling rod balance time, longer balance beam traversal time, elevated MDA level and α-syn expression, as well as decreased levels of SOD, GSH-Px and reduced expressions of TH, Nrf2, and NAD(P)H quinone dehydrogenase 1 (NQO1) (all P<0.05). Compared with the PD group, the QUE-L and QUE-H groups presented relatively ordered arrangement of nigral dopaminergic neurons, increased number of neurons with relatively normal morphology, more Nissl bodies, higher suspension test scores, longer rolling rod balance time, shorter balance beam traversal time, decreased MDA level and α-syn expression, as well as elevated levels of SOD, GSH-Px and increased expressions of TH, Nrf2, and NQO1 (all P<0.05). Compared with the QUE-H group, the QUE-H+ML385 group exhibited disorganized arrangement of dopaminergic neurons, significantly reduced number of neurons with abnormal morphology, markedly decreased number of Nissl bodies, lower suspension test scores, shorter rolling rod balance time, longer balance beam traversal time, increased MDA level and α-syn expression, as well as reduced levels of SOD, GSH-Px and decreased expressions of TH, Nrf2, and NQO1 (all P<0.05). Conclusion: QUE can improve motor behavioral disorders in PD mice, and the mechanism may be related to the activation of the Nrf2-ARE signaling pathway.