Aim： Carvacrol （2-methyl-5-isopropylphenol）, a phenolic monoterpene in the essential oils of the genera Origanum and Thymus, has been shown to exert a variety of therapeutic effects. Here we examined whether carvacrol protected neuroblastoma SH-SY5Y cells against Fe2＋-induced apoptosis and explored the underlying mechanisms. Methods： Neuroblastoma SH-SY5Y cells were incubated with Fe2＋ for 24 h, and the cell viability was assessed with CCK-8 assay. TUNEL assay and flow cytometric analysis were performed to evaluate cell apoptosis. The mRNA levels of pro-inflammatory cytokines and NF-KB p65 were determined using qPCR. The expression of relevant proteins was determined using Western blot analysis or immunofluorescence staining. Results： Treatment of SH-SY5Y cells with Fe2＋ （50-200 pmol/L） dose-dependently decreased the cell viability, which was significantly attenuated by pretreatment with carvacrol （164 and 333 pmol/L）. Treatment with Fe2＋ increased the Bax level and caspase-3 activity, and decreased the Bcl-2 level, resulting in cell apoptosis. Furthermore, treatment with Fe2＋ significantly increased the gene expression of IL-1β, IL-6 and TNF-α, and induced the nuclear translocation of NF-KB. Treatment with Fe2. also significantly increased the phosphorylation of p38, ERK, JNK and IKK in the cells. Pretreatment with carvacrol significantly inhibited Fe2＋-induced activation of NF-KB, expression of the pro-inflammatory cytokines, and cell apoptosis. Moreover, pretreatment with carvacrol inhibited Fe2＋-induced phosphorylation of JNK and IKK, but not p38 and ERK in the cells. Conclusion： Carvacrol protects neuroblastoma SH-SY5Y cells against Fe2＋-induced apoptosis, which may result from suppressing the MAPK/JNK-NF-KB signaling pathways.