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Pyrogallol (PG) induces apoptosis in lung cancer cells via the overproduction of O 2  •- and affects mitogen-activated protein kinases (MAPKs) in these cells. The aim of the present study was to elucidate the effect of PG and/or MAPK inhibitors on human pulmonary fibroblast (HPF) cell viability in relation to reactive oxygen species (ROS) and glutathione (GSH). Treatment with 50 or 100 µM PG inhibited the viability of HPF cells, and induced cell death and the loss of mitochondrial membrane potential (MMP; ΔΨ m ). In particular, treatment with 100 µM PG induced cell death via apoptosis as well as necrosis in HPF cells. PG increased mitochondrial O 2  •- levels and the number of GSH-depleted HPF cells. All the MAPK (mitogen-activated protein kinase kinase, c-Jun N-terminal kinase and p38) inhibitors enhanced the inhibition of cell viability, cell death and MMP (ΔΨ m ) loss in 100 µM PG-treated HPF cells. All the inhibitors increased the O 2 •- levels in 100 µM PG-treated HPF cells, but none of the inhibitors significantly altered the PG-induced GSH depletion. In conclusion, PG treatment induced cell death via apoptosis and necrosis in HPF cells. Treatment with MAPK inhibitors slightly enhanced cell death in PG-treated HPF cells. HPF cell death induced by PG and/or MAPK inhibitors was at least partially associated with changes in O 2 •- levels and GSH content. The present data provided useful information to understand PG-induced normal lung cell death in association with MAPK signaling pathways and ROS levels.

MAPK inhibitors enhance cell death in pyrogallol-treated human pulmonary fibroblast cells via increasing O2•− levels