BACKGROUND
Erythromycin and its derivatives have been used to treat nasal polyposis and reduce
inflammation, but the mechanism of action remains unclear. The
extracellular signal-regulated kinase (ERK) and
mitogen-activated protein kinase (MAPK) pathway
proteins are expressed in
nasal polyps. The aim of this study was to investigate the effects of
erythromycin on cell proliferation, apoptosis, and the expression of p-MEK1 and p-ERK1 on cultured
nasal polyp-derived cells. MATERIAL AND METHODS
Nasal polyp-derived cells (n=32) and control cells from normal inferior turbinate tissue (n=32) were divided into four groups: the control group; the
erythromycin-treated (100 μM) group; the
selumetinib-treated (2 nM) group; and the
erythromycin +
selumetinib-treated group. Western blot was used to detect p-MEK1 and p-ERK1
proteins. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect
mRNA expression of BCL-2 and BAX. Flow cytometry detected expression of Ki-67 and cell apoptosis. Cell apoptosis was evaluated by
terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL). Spectrophotometry assessed
caspase-3 activity. RESULTS The expression of Ki-67 was significantly increased, and cell apoptosis was significantly reduced in untreated
nasal polyp-derived cells compared with controls.
Erythromycin treatment significantly decreased cell proliferation and the expression of p-MEK1 and p-ERK1, and increased apoptosis in
nasal polyp-derived cells compared with control cells.
Selumetinib treatment had a synergistic effect with
erythromycin to reduce the expression of p-MEK1 and p-ERK1, reduce cell proliferation, and increase cell apoptosis. CONCLUSIONS In cultured cells derived from
nasal polyps,
erythromycin treatment reduced cell proliferation and increased apoptosis by inhibiting the activation of the ERK/MAPK signaling pathway.