Fibroblasts usually mediate acute wound healing and long-term tissue remodeling with scarring in tissue injury. In myocardial infarction (MI), following a prolonged lack of oxygen supply, necrotized cardiomyocytes become replaced by secreted extracellular matrix proteins produced by fibroblasts. Dendritic cells (DCs) act as inflammatory cells and can migrate from the bone marrow to the infarct areas and infarct border areas to mediate collagen accumulation after MI, whereas trichostatin A (TSA) can regulate the apoptosis and proliferation of the fibroblasts and affect DCs functions under oxygen–glucose deprivation (OGD) conditions. In this study, we used proteomics to investigate the effects of TSA and bone marrow-derived dendritic cells (BMDCs) on NIH3T3 fibroblasts under OGD conditions. Results showed that the fatty acid degradation pathway was significantly upregulated in NIH3T3 cells under OGD conditions, and the fatty acid synthesis pathway was significantly downregulated in NIH3T3 cells treated with BMDCs conditioned media with TSA (BMDCs-CM[TSA]) under OGD conditions. Meanwhile, the BMDCs-CM(TSA) significantly decreased the levels of triglycerides and free fatty acids and mediated ten fatty acid metabolism-related proteins in the NIH3T3 cells under OGD conditions. Summarily, the proteomic analysis showed that TSA and BMDCs affect fatty acid metabolism in NIH3T3 cells under OGD conditions.