Background: Although air pollution containing fine dust particles is gaining attention worldwide, little is known about the effects of such pollutants on diabetic wounds. Air pollutants from diesel exhaust particles (DEPs) cause inflammation, resulting in an increased expression of pro-inflammatory cytokines and chemo- kines, which attract monocytes and T cells to the sites of inflamma- tion. The authors evaluated the effects of air pollutants on diabetic wounds.
Materials and methods: Fibroblast cells were derived from streptozotocin-induced diabetic rats. Cell Counting Kit-8 assays were used to determine cell viability. The expression of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), cyclooxygen- ase-2 (COX-2), and interleukin-6 (IL-6) was evaluated by reverse transcription polymerase chain reaction and western blot analysis.
Results: The proliferation of DEP-treated fibroblasts decreased with time. The messenger ribonucleic acid expression of TNF-α and COX- 2 in DEP-treated fibroblasts increased in both normal and diabetic fibroblasts, while IL-6 expression remained unchanged. The protein expression of TNF-α, COX-2, and IL-6 in DEP-treated fibroblasts increased compared to samples not exposed to DEP.
Conclusions: Diesel exhaust particles regulate the expression of pro-inflammatory cytokines such as IL-6, TNF-α, and COX-2, which may impede dia- betic healing in vitro.