MAPK inhibitors differentially affect gallic acid-induced human pulmonary fibroblast cell growth inhibition
Affiliations: Department of Physiology, Institute for Medical Sciences, Chonbuk National University Medical School, Jeonju 561-180, Korea
- Published online on: September 10, 2010 https://doi.org/10.3892/mmr.2010.361
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Gallic acid (GA) has various biological properties, including an anti-cancer effect. However, little is known about the toxicological effect of GA in primary normal cells in relation to mitogen-activated protein kinase (MAPK) signaling. In this study, we investigated the effects of MAPK (MEK, JNK or p38) inhibitors on GA-treated human pulmonary fibroblast (HPF) cells in relation to cell growth inhibition, cell death, reactive oxygen species (ROS) and glutathione (GSH). GA induced HPF cell growth inhibition and cell death at 24 h, which was accompanied by the loss of mitochondrial membrane potential (MMP; ∆ψm). GA increased ROS levels and GSH-depleted cell numbers in the HPF cells. The MEK inhibitor did not affect cell growth inhibition, cell death, ROS and GSH levels in the GA-treated HPF cells. The JNK inhibitor slightly enhanced cell growth inhibition by GA, while the p38 inhibitor significantly prevented the growth inhibition. Both JNK and p38 inhibitors did not affect cell death, ROS and GSH levels in the GA-treated HPF cells. In conclusion, MAPK inhibitors differentially affected the growth inhibition of GA-treated HPF cells, which were not related to cell death, ROS and GSH levels.