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Tunicamycin (TCM or TM) [1] [2] is an antibiotic. It can block the reaction between UDP-N-acetylglucosamine and dolichol phosphate in the first step of glycoprotein synthesis and thus inhibit the synthesis of all N-linked glycoproteins, finally cause endoplasmic reticulum (ER) stress [3]. In Bacillus subtilis cells, the IC50 for TCM to inhibit the formation of dolichyl pyrophosphoryl N-acetylglucosamine (Dol-p-p-GlcNAc) is 0.03 μg/ml [2].

The ER stress response is a potent, evolutionarily conserved response to cellular metabolic stress and misfolded proteins. ER stress is induced by disruption of ER functions, such as transport to the Golgi complex or protein glycosylation, or by disturbances in the ER lumen environment, such as redox status or altered calcium homeostasis [3].

In RAW264.7 cells, tunicamycin significantly reduced LPS-induced nitrite release/production and attenuated the expression of mRNAs and hence proteins of COX-2 and iNOS. In addition, tunicamycin at a concentration of 0.5 μg/ml did not have any effect on cell survival/proliferation, but at 48h tunicamycin provided protection against activation-induced macrophage cell death. In a concentration-dependent manner, tunicamycin reduced COX-2 and iNOS protein expressions in response to LPS and induced a concurrent increase in 78-kDa glucose-regulated protein (GRP78), an ER chaperone [3].

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