Abstract: This study employed microdialysis sampling coupled with high-resolution gas chromatography-mass spectrometry to analyze the transdermal components of Jianpi Patch (JPT), and combined pharmacodynamics, network pharmacology, and molecular docking to investigate the effects and mechanisms of its acupoint (Shenque and Zhongwan) application in the treatment of pediatric functional dyspepsia (PFD). Pharmacodynamic results showed that compared with the model group, the high-dose JPT group exhibited significant increases in serum gastrin (GAS) and motilin (MTL) levels, as well as significant decreases in gastric inhibitory polypeptide (GIP) and somatostatin (SS) levels. In both high- and low-dose JPT groups, mast cell counts in acupoint skin were markedly reduced, inflammatory cell infiltration in the gastric antrum mucosa was alleviated, and substance P (SP) expression in acupoint skin was decreased. A total of 66 transdermal components were identified by high-resolution gas chromatography-mass spectrometry, mainly terpenoids and hydrocarbons. Network pharmacology screened 350 drug targets, which intersected with 3, 261 FD-related targets to yield 197 common targets. A component–target network was constructed, identifying myrtenyl acetate, cyclohexyl acetate, (−)-verbenone, and eugenol as potential active ingredients. Protein–protein interaction network analysis identified hub targets including SRC, ESR1, JUN, AKT1, CTNNB1, MAPK3, and PIK3R1. KEGG enrichment analysis indicated that these targets were mainly involved in the PI3K-Akt signaling pathway and other pathways. Molecular docking showed good binding affinity between the core components and hub targets. Immunohistochemistry confirmed that JPT upregulated the protein expression of PIK3R1, PI3K, AKT, and c-Kit, and downregulated EGFR and GFAP expression in the gastric antrum. The findings of this study suggest that JPT may improve PFD by participating in the regulation of signal transmission of gastrointestinal neurotransmitters such as substance P and by modulating signaling pathways such as PI3K-Akt.