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.