To observe the effect of acupuncture and moxibustion on the expression of proteins involved in the interleukin-17 receptor A(IL-17RA)/nuclear factor-κB(NF-κB) signaling pathway in the midbrain substantia nigra of mice with Parkinson's disease and to explore the possible mechanism of acupuncture and moxibustion in relieving the symptoms of Parkinson's disease.Methods:The specific pathogen free(SPF)-grade 8-week-old male C57BL/6 mice were randomly assigned into a blank group,a model group,an acupuncture group,an acupuncture+moxibustion group,and a rasagiline group.The mouse model of Parkinson's disease was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP).The acupuncture was carried out at the Baihui(GV 20) and Yanglingquan(GB 34) and the moxibustion at Guanyuan(CV 4).Rasagiline was administrated by gavage.The overall rod performance(ORP) of mice was scored.The expression of tyrosine hydroxylase(TH) and alpha-synuclein(α-syn) in the substantia nigra was detected by immunofluorescence staining,and the protein levels of IL-17RA and downstream molecules in the substantia nigra were determined by Western blotting.Results:Compared with the blank group,the modeling decreased the ORP score and TH expression,while such decreases were recovered by acupuncture and/or moxibustion(P<0.05).The model group had higher fluorescence intensity of α-syn,higher level of NF-κB inhibitor-alpha(IκBα),and higher p-IκBα/IκBα ratio in the substantia nigra than the blank group(P<0.05).Compared with the model group,acupuncture,acupuncture+moxibustion,and rasagiline decreased the immunofluorescence intensity of α-syn(P<0.05) as well as the expression of p-IκBα and the p-IκBα/IκBα ratio.Acupuncture+moxibustion down-regulated the IL-17RA expression(P<0.05).Conclusion:Acupuncture and moxibustion may improve the rod performance,protect TH-positive neurons in the substantia nigra,and inhibit the expression of α-syn of the mice with Parkinson's disease by regulating IL-17 receptor signaling pathway,especially the phosphorylation of IκBα.