earticle

영어

Tunicamycin is an antibiotic that blocks the synthesis of all N-linked glycoproteins. It causes endoplasmic reticulum (ER) stress and induce unfolded protein response (UPR). Recent evidence suggests tunicamycin-inducd ER stress is a possible cause of inflammation. In the present study, we have investigated the role of tunicamycin on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 macrophage. Tunicamycin decreaced inducible nitric oxide synthase (iNOS), Cyclooxygenase-2 (COX-2), and pro-inflammatory cytokine such as interleukin 1 beta (IL-1β) and tumor necrosis factor alpa (TNF-α) expression in response to LPS in RAW264.7 macrophage cells. However, other well-known ER stress inducers, A23187 and Thapsigargin increased LPS-induced COX-2 expression and had no effect on LPS-induced iNOS, TNF-α and IL-1β expression. These results suggest that the inhibitory effect of tuncimaycin on LPS-induced inflammation is independent of its effect on ER stress induction. We further demonstrated that tunicamycin inhibited LPS-induced NF-κB activation. in RAW264.7 macrophage cells.