Abstract
++ exchangers (NHEs) are activated by various stimuli and regulate the functions of macrophages. The NHE inhibitors amiloride, 5-(NN-dimethyl)-amiloride (DMA) and 5-(N-ethyl-N-isopropyl)amiloride (EIPA) inhibited the lipopolysaccharide (LPS)-induced production of prostaglandin (PG) E2 in the mouse macrophage-like cell line RAW 264. They inhibited both the LPS-induced release of arachidonic acid from membrane phospholipids at 4 h and the LPS-induced increase in the level of cyclooxygenase (COX)-2 protein at 6 h, but did not directly inhibit the COX activity. The vacuolar-type (H + )-ATPase (V-ATPase) inhibitor, bafilomycin A1, which activates NHE via reducing intracellular pH, also increased the level of COX-2 protein. The bafilomycin A1-induced expression of COX-2 was inhibited by the NHE inhibitors and by the Na
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