Mechanistically, compared to previous research studies on the main constituents for the treatment of PID by relieving the degree of fibrosis in the uterus via ERK1/2 and TGFβ-SMAD2/3 signaling pathways, we reported the critical active compounds and relevant binding modes of IL-17 signaling pathway and Th17 cell differentiation-related targets in the treatment of PID by inhibiting inflammatory factors, antitissue fibrosis, and microbial growth. Here, TGFB1 is linked to pelvic inflammatory disease.