Purpurogallin exerts anti‑inflammatory effects in lipopolysaccharide‑stimulated BV2 microglial cells through the inactivation of the NF‑κB and MAPK signaling pathways.

In this study, we investigated the inhibitory effects of purpurogallin, a naturally occurring phenol, on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators and cytokines in BV2 microglia cells. The cells were pre-treated or not with various concentrations of purpurogallin and then stimulated with 0.5 µg/ml LPS. Cell viability was measured by MTT assay. We also measured the production of nictric oxice (NO) and prostaglandin E2 (PGE2). Our data indicated that treatment with purpurogallin significantly inhibited the excessive production of NO and PGE2 in LPS-stimulated BV2 microglial cells. These inhibitory effects were associated with the downregulation of key enzymes for NO and PGE2, inducible NO synthase (iNOS) and cyclooxygenase-2 (COX2) expression, respectively. Purpurogallin also attenuated the production of pro-inflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) by suppressing their mRNA and protein expression. The molecular mechanisms underlying the purpurogallin-mediated attenuation of inflammation in BV2 cells closely correlated with the suppression of the translocation of the nuclear factor-κB (NF-κB) p65 subunit into the nucleus and the degradation of the inhibitor of NF-κB (IκB). Moreover, purpurogallin exhibited anti-inflammatory properties by suppressing the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase signaling pathways. These findings suggest that purpurogallin exerts neuroprotective effects through the suppression of pro-inflammatory pathways in activated microglia.