ObjectiveTo investigate the pharmacological basis and mechanism of Qinlian Jiangxia decoction （QLJXD） in the treatment of glucose and lipid metabolism disorders. MethodsThe Encyclopedia of Traditional Chinese Medicine （ETCM） and the GeneCards database were used to predict the active components and targets of QLJXD in the treatment of type 2 diabetes mellitus （T2DM） combined with dyslipidemia. The key components and core targets were screened following protein-protein interaction （PPI） network， Gene Ontology （GO）， and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses of the targets and then verified by molecular docking. SD rats were used to prepare the QLJXD-medicated serum， and a 3T3-L1 adipocyte model of insulin resistance （IR） was constructed with 1 μmol·L^-1 dexamethasone （DEX）. After intervention with four sera， cell glucose consumption and lipid metabolism levels were measured to screen the optimal action concentration of the medicated serum. A 3T3-L1 adipocyte model of IR with fatty acid-binding protein 4 （FABP4） overexpression was further constructed by plasmid transfection. Western blot and Real-time quantitative PCR （Real-time PCR） were employed to determine the expression of FABP4 and peroxisome proliferator-activated receptor γ （PPARG） at protein and mRNA levels， respectively， on the basis of which the regulatory effect of QLJXD on the FABP4/PPARG pathway was evaluated. ResultsNetwork pharmacology revealed that the key active components of QLJXD in treating T2DM complicated with dyslipidemia were baicalein， acacetin， and α-linolenic acid， and FABP1， FABP4， and PPARG were the core targets. Molecular docking showed good binding activity between the key components and core targets. QLJXD-medicated serum improved the glucose uptake capacity， increased insulin （INS）-stimulated glucose consumption （P<0.01）， and reduced total cholesterol （TC）， triglyceride （TG）， and free fatty acid （FFA） levels （P<0.01） in the 3T3-L1 adipocyte model of IR， with the medium-dose-medicated serum demonstrating the most potent effects. Overexpression of FABP4 impaired the glucose uptake capacity in the 3T3-L1 adipocyte model of IR and promoted intracellular accumulation of TC， TG， and FFA （P<0.05）. The medium-dose-medicated serum improved glucose uptake capacity and reduced the accumulation of TC， TG， and FFA （P<0.01）， while decreasing the protein and mRNA expression levels of FABP4 and concomitantly increasing the protein and mRNA levels of PPARG （P<0.05） in the 3T3-L1 adipocyte model of IR with FABP4 overexpression. ConclusionThe QLJXD-medicated serum has been evidenced to ameliorate glucose and lipid metabolism disorders in the 3T3-L1 adipocyte model of IR through multiple components， with the mechanism related to the FABP4/PPARG signaling pathway.