目的 借助粪菌移植研究姜黄素改善帕金森病（PD）小鼠行为缺陷的作用机制。 方法 腹腔注射 1-甲-基-4-苯基-1，2，3，6-四氢吡啶(MPTP)建立小鼠亚急性PD模型，收集分离模型组和80mg/kg姜黄素（Cur）模型治疗组小鼠粪便菌群。通过粪菌移植处理，将小鼠分为粪便菌群溶剂移植组（FMTcon）、模型粪便菌群移植组（FMTmodel）、MPTP模型组（model）以及模型加姜黄素粪便菌群移植组（model+FMTCur）4组。通过转棒、爬杆和旷场实验评估小鼠运动能力，通过免疫荧光观察动物脑黑质部位酪氨酸羟化酶（TH）阳性神经元表达，并检测小鼠中脑部位肿瘤坏死因子α（TNF-α）基因表达，核因子κB ( NF-κB)和核苷酸结合寡聚结构域样受体蛋白 3 (NLRP3) 通路相关蛋白表达。 结果 成功建立小鼠亚急性PD动物模型，收集分离粪便菌群。Model组表现为明显运动障碍，表现转棒维持时间缩短（P＜0.05），爬杆时间延长（P＜0.05），旷场内总运动距离（P＜0.001）和中心区运动时间（P＜0.01）明显缩短；黑质部位TH阳性神经元相对表达量显著降低(P＜0.01)；中脑内TNF-α mRNA表达显著升高(P＜0.01)，NF-κB（P＜0.001）、磷酸化NF-κB（p-NF-κB）（P＜0.01）、NLRP3（P＜0.001）、Caspase-1（P＜0.01）蛋白表达均明显升高。模型粪便菌群移植组（FMTmodel）也出现运动障碍，表现为转棒时间缩短，爬杆时间延长趋势，旷场内总运动距离明显下降（P＜0.01）和中心区运动时间缩短趋势；黑质部位TH阳性神经元相对表达量明显下降(P＜0.05)；中脑内TNF-α mRNA表达明显升高(P＜0.01)，NF-κB（P＜0.05）和Caspase-1(P＜0.01)蛋白表达均明显升高。经姜黄素治疗组粪便菌群移植小鼠（model+FMTCur）运动能力有改善，表现为爬杆时间缩短（P＜0.05），转棒维持时间（P＜0.01）和中心区域运动时间（P＜0.05）明显延长；黑质部位TH阳性神经元相对表达量明显增多(P＜0.05)；中脑内TNF-α mRNA表达明显降低(P＜0.01)，NF-κB（P＜0.001）、p-NF-κB（P＜0.01）、NLRP3（P＜0.05）、Caspase-1（P＜0.01）蛋白表达均明显降低。结论 PD模型小鼠粪菌移植会引起小鼠行为缺陷，黑质部位TH阳性神经元损伤，激发脑内神经炎症；姜黄素治疗后粪菌移植可以改善帕金森模型小鼠的行为缺陷，逆转黑质部位TH阳性神经元损伤，减少脑内神经炎症因子，降低NF-κB和NLRP3通路相关蛋白表达，表明姜黄素改善小鼠帕金森行为缺陷可能通过调节肠道菌群来实现。

 Objective To explore the mechanism by which curcumin improves behavioral deficits in mice with Parkinson’s disease(PD) through fecal microbiota transplantation.   Methods A subacute model of PD in mice was induced by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Fecal microbiota from both the model group and the curcumin(Cur)-treated group (80 mg/kg) were collected and analyzed. The experiment involving fecal microbiota transplantation was structured into four distinct groups, fecal microbiota solvent transplantation group (FMTcon), model fecal microbiota transplantation group (FMTmodel), MPTP-induced model group (model), and model group subjected to fecal microbiota transplantation following curcumin treatment (model+FMTCur). The motor skills of the mice were assessed by using rod rotation, pole climbing experiment, and open field tests. Immunofluorescence techniques were employed to observe the expression tyrosine hydroxylase (TH)-positive neurons in the substantia nigra of the brain. Additionally, the gene expression of tumor necrosis factor-α (TNF-α) in the midbrain of mice was analyzed, alongside the protein expression of nuclear factor-κB(NF-κB) and nucleotide binding oligomerization domain-like receptor protein 3 (NLRP3).   Results The subacute PD animal model in mice was successfully established, and fecal microbiota were separated and gathered. The model group exhibited significant motor impairment, as evidenced by a shortened rod rotation time (P<0.05), prolonged pole climbing time (P<0.05), significantly reduced total movement distance within the open field (P<0.001), and decreased time spent in the central zone (P<0.01). The relative expression level of TH+ neurons in the substantia nigra was significantly reduced (P<0.01). Moreover, mRNA expression of TNF-α in the midbrain increased significantly(P<0.01), along with significant elevations in protein expression of NF-κB (P<0.001), phosphorylated NF-κB (p-NF-κB) (P<0.01), NLRP3 (P<0.001), and Caspase-1 (P<0.01).The transplanted model microbial group (FMTmodel) also exhibited motor impairment, manifested by a trend of shortened rod rotation time, prolonged pole climbing time, a significant decrease in total movement distance within the open field (P<0.01), and a trend of shortened time spent in the central zone. The relative expression level of TH⁺ neurons in the substantia nigra decreased significantly(P<0.05). Additionally, mRNA expression of TNF-α in the midbrain increased significantly(P<0.01), along with notable elevations in the protein expression of NF-κB (P<0.05), and Caspase-1 (P<0.01).Treatment with curcumin in the fecal microbiota transplantation group of mice (model+FMTCur) showed improvements in motor abilities, evidenced by shortened pole climbing time (P<0.05), significantly prolonged rod rotation time (P<0.01), and extended time spent in the central zone (P<0.05). The relative expression level of TH+ dopaminergic neurons in the substantia nigra increased significantly(P<0.05). Moreover, mRNA expression of TNF-α in the midbrain decreased significantly(P<0.01), along with notable reductions in the protein expression of NF-κB (P<0.001), p-NF-κB (P<0.01), NLRP3 (P<0.05), and Caspase-1 (P<0.01).   Conclusion Fecal microbiota transplantation in PD model mice can induce behavioral deficits, damage TH+ neurons in the substantia nigra, and trigger neuroinflammation in the brain. Subsequent curcumin treatment can ameliorate these deficits, reverse damage to TH+ neurons, reduce neuroinflammatory factors, and decrease the expression of NF-κB and NLRP3 pathways. This preliminary evidence suggests that curcumin may improve Parkinsonian behavioral deficits in mice by modulating the gut microbiota.