目的  探讨脱落酸（ABA）对1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森病（PD）模型小鼠的神经保护作用及机制。   方法 选取8周龄C57BL/6J小鼠，随机分为对照组(Ctrl)、MPTP组和MPTP+ABA组，每组12只。除对照组外，其余小鼠腹腔注射MPTP 25 mg/（kg·d），连续8 d构建PD亚急性模型。MPTP+ABA组于创建模型前3 d起，每天腹腔注射ABA 25 mg/（kg·d），连续11 d。末次给药后24 h进行行为学检测，第3天通过Western blotting检测小鼠黑质致密部(SNc)与纹状体(STR)的酪氨酸氢化酶（TH）和胶质纤维酸性蛋白（GFAP）的表达，Real-time PCR检测炎症因子mRNA水平；通过免疫荧光染色检测TH、GFAP和离子化钙结合适配分子1（Iba1）的表达。   结果  与对照组相比，MPTP组小鼠运动功能受损，黑质致密部TH阳性多巴胺能神经元数量减少，黑质致密部和纹状体中TH蛋白表达下调，GFAP蛋白表达上调，GFAP、Iba1阳性细胞数量增加，促炎因子表达水平升高；相比MPTP组，MPTP+ABA组小鼠的运动功能改善，黑质致密部TH阳性神经元数量增加，黑质致密部和纹状体中TH蛋白表达水平升高，GFAP蛋白表达水平降低，GFAP、Iba1阳性细胞数量减少，促炎因子表达水平降低。  结论  ABA可改善MPTP诱导的帕金森病模型小鼠的运动功能，减少黑质致密部多巴胺能神经元变性死亡，抑制黑质致密部及纹状体星形胶质细胞和小胶质细胞的增殖活化，减轻神经炎症反应，提示ABA对MPTP诱导的PD模型小鼠具有神经保护作用。

Objective To investigate the neuroprotective effects and mechanisms of abscisic acid (ABA) in 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson’s disease (PD) mouse models.   Methods Eight-week-old C57BL/6J mice were randomly divided into three groups, control group (Ctrl), MPTP group, and MPTP+ABA group, 12 mice in each group. Except for the control group, mice in the other groups were intraperitoneally injected with MPTP 25 mg/kg daily for 8 consecutive days to establish a subacute PD model. The MPTP+ABA group received intraperitoneal injections of ABA 25 mg/kg daily for 11 consecutive days, starting 3 days prior to MPTP administration. Behavioral tests were performed 24 hours after the last administration. On day 3, the expression of tyrosine hydroxylase (TH) and glial fibrillary acidic protein (GFAP) in the substantia nigra pars compacta (SNc) and striatum (STR) was analyzed by Western blotting, and mRNA levels of inflammatory factors were measured by Real-time PCR. Immunofluorescent staining was used to detect the expression of TH, GFAP, and ionized calciumbinding adapter molecule 1 (Iba1).    Results Compared with the control group, MPTP-treated mice exhibited impaired motor function, a reduced number of TH-positive dopaminergic neurons in the SNc, down-regulated TH protein expression in both the SNc and striatum, up-regulated GFAP protein expression, increased numbers of GFAP-and Iba1-positive cells, and elevated levels of pro-inflammatory factors. In contrast, the MPTP+ABA group showed improved motor function, increased TH-positive neurons in the SNc, up-regulated TH protein expression, down-regulated GFAP protein expression, reduced numbers of GFAP-and Iba1-positive cells, and decreased pro-inflammatory factor levels compared to the MPTP group.   Conclusion  ABA ameliorates motor dysfunction in MPTP-induced PD model mice, reduces degeneration and death of dopaminergic neurons in the SNc, suppresses the proliferation and activation of astrocytes and microglia in the SNc and striatum, and alleviates neuroinflammation. These results suggest that ABA exerts neuroprotective effects in MPTP-induced PD model mice.