Nonsteroidal anti-inflammatory drugs (NSAIDs), one of which is diclofenac sodium, are widely used in clinical practice. This study aimed to assess the effect of diclofenac sodium on bone marrow cellularity, the population of hematopoietic stem and progenitor cells (Lin−Sca-1+ c-Kit+, LSK), as well as the levels of tumor necrosis factor — (TNFa) and interleukin-1b (IL1b) in laboratory mice with experimental dermatitis. The study was a randomized controlled trial; the experimental phase lasted 96 hours. Male BALB/c mice (n = 6, age 46 weeks, 18–25 g) were randomized into five groups: intact, untreated dermatitis, dermatitis + diclofenac 1.5 mg/kg, dermatitis + diclofenac 3 mg/kg, diclofenac 3 mg/kg without dermatitis. The drug was administered intramuscularly 2 times a day for 96 hours. Dermatitis was modeled using sodium dodecyl sulfate and Dermatophagoides farinae. Bone marrow was collected after 96 hours. The total number of cells was determined by an automatic counter, the LSK cell population by flow cytometry, and cytokine concentrations by ELISA. Statistical analysis was performed using ANOVA (p < 0.05). We observed a decrease in bone marrow cellularity in dermatitis groups (0.95 ± 0.12 versus 1.20 ± 0.15 × 106 ml; p < 0.05). Diclofenac 1.5 mg/kg decreased cellularity moderately (0.80 ± 0.10 × 106 ml) and an increased LSK cells (3.8 ± 0.5% vs. 2.1 ± 0.3%; p < 0.05). Diclofenac 3 mg/kg markedly brought down cellularity (0.60 ± 0.08 × 106/ml) and LSK cells (1.4 ± 0.3%; p < 0.01), and brought up IL1b (15.5 ± 1.2 pg/ml) and TNFa (82.1 ± 4.5 pg/ml). Our findings indicate a dose-dependent effect of diclofenac sodium on hematopoiesis and inflammatory response.