Abstract
Isaindigotone possesses extensive pharmacological activities, including anti‑inflammatory effects. The present study investigated the role of isaindigotone in the inhibition of neuroinflammation. Mouse BV‑2 cells were incubated with lipopolysaccharide (LPS; 1 mg/l) for 24 h in a microglial inflammatory model in vitro. The effects of isaindigotone on BV‑2 cell proliferation were observed using the 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide method. Following co‑incubation, an enzyme‑linked immunosorbent assay and western blot analysis were used to analyze cellular levels of cytokines and associated protein expression, including the phosphorylation of nuclear factor (NF)‑κB. The effects of isaindigotone concentration on LPS‑mediated cell chemotaxis behavior were assessed using a chemotaxis assay. The results indicated that isaindigotone is non‑toxic towards BV‑2 cells. Compared with the LPS group, isaindigotone significantly reduced the secretion of tumor necrosis factor‑α and interleukin‑1β in BV‑2 cells and reduced the cell chemotaxis caused by LPS; it also reversed morphological changes in the BV‑2 cells and inhibited the phosphorylation of NF‑κB. The results of the present study suggest that isaindigotone can inhibit inflammatory reactions in LPS‑induced BV‑2 cells, and provides a theoretical basis and experimental evidence for examining the mechanism underlying the isaindigotone‑induced inhibition of neuroinflammation.