To observe the effect of Qianliexiao Decoction on the regulation of the transforming growth factor-β1(TGF-β1)-Smad homolog 2/3(Smad2/3) signaling pathway in the differentiation of Th17 cells in experimental autoimmune prostatitis(EAP).Methods:A total of 120 specific-pathogen-free(SPF) male C57BL/6 mice were randomly divided into six groups:blank group,model group,positive control(pirfenidone) group,and low,medium,and high dose Qianliexiao Decoction groups,with 20 mice in each group.An EAP mouse model with dampness-heat syndrome was established through immune adjuvant combined with traditional Chinese medicine(TCM) dampness-heat factors.After model establishment,the corresponding treatments were administered.Hematoxylin-eosin(HE) staining was used to observe pathological changes in the prostate and spleen tissues.Real-time quantitative reverse transcription polymerase chain reaction(RT-PCR) and Western Blotting(WB) analysis were used to detect the expression levels of TGF-β1,TGF-β1 receptor I(TGF-β1RⅠ),interleukin 17-A(IL-17A),retinoid-related orphan receptor γt(RORγt),phosphorylated Smad2(p-Smad2),Smad2,phosphorylated Smad3(p-Smad3),and Smad3 mRNA and protein in prostate tissue.Results:Compared with the blank group,the model group showed significantly increased prostate index and dampness-heat syndrome scores,and extensive infiltration of inflammatory cells in the prostate and spleen tissues,indicating successful establishment of the EAP model in mice with dampness-heat syndrome.The expression levels of TGF-β1,TGF-β1RⅠ,IL-17A,RORγt,p-Smad2,and p-Smad3 were significantly increased(P<0.05).Compared with the model group,both the pirfenidone group and all doses of the Qianliexiao Decoction groups showed varying degrees of improvement in inflammatory infiltration,with significantly reduced expression of TGF-β1,TGF-β1RⅠ,IL-17A,RORγt,p-Smad2,and p-Smad3(P<0.05).Conclusion:Qianliexiao Decoction can effectively inhibit the abnormal differentiation of Th17 cells in EAP,and its mechanism of action may be related to the TGF-β1-Smad2/3 signaling pathway.