antiinflammatory effects of novel thiazolidinone derivatives as bioactive heterocycles on raw264.7 cells

The inhibition of the inducible nitric oxide synthase (inos), cyclooxygenase 2 (cox-2) and nuclear factor-κb (nf-κb) production are research targets of attract in the field of anti-inflammatory drug development. therefore, this study was designed to investigate the anti-inflammatory effects of novel thiazolidinone derivatives using a cellular model of lipopolysaccharide (lps)-stimulated murine macrophage raw 264.7. in the present study, five new derivatives (a to e) of thiazolidinone were synthesized and screened for anti-inflammatory activities. cell viability of lps-stimulated raw 264.7 macrophages clearly decreased in >55 μg/ml of synthesized a-e compounds especially in the presence of c; therefore, up to 50 μg/ml of compounds were selected for the subsequent analysis. a majority of these compounds showed significant inhibition on the production of no in lps-stimulated macrophages in a dose-dependent manner. compounds b and d (10-50 μg/ml) significantly inhibited lps-induced nf-κb (p65) production in a dose-dependent manner. the effects of b and d on inos and cox-2 mrna and protein expression in lps-stimulated raw 264.7 cells were detected by real time-pcr and western blot. b derivative significantly suppressed the inos and cox-2 mrna level and as well as protein expression. taken together, these results reveal that compound b as new thiazolidinone derivative decreased expression of the inflammatory-related signals (no, inos and cox-2) through regulation of nf-κb; hence, this compound could be suggested as a novel therapeutic strategy for inflammation-associated disorders.