The present study investigated the effect of berberine (BBR) on amyloid β 25-35 (Aβ25-35)-induced inflammatory response in human neuroblastoma cells. To model the inflammatory response observed in the central nervous system of patients with Alzheimer's disease, SH-SY5Y and SK-N-SH neuroblastoma cells were induced by Aβ25-35 (5 µM) for 24 h. Subsequently, cells were treated with BBR or indomethacin for 2 h. The cell survival rate was determined by the MTT assay. The activity of lactate dehydrogenase (LDH) in the cell culture medium was examined by spectrophotometry. The expression levels of inflammatory factors prostaglandin E2 (PGE2) and tumor necrosis factor-α (TNF-α) were determined by ELISA assays. The mRNA and protein expression levels of interleukin (IL)-1β, cyclooxygenase 2 (COX-2) and tumor necrosis factor receptor 1 (TNFR1) were measured by reverse-transcription-quantitative polymerase chain reaction and Western blotting, respectively. The results indicated that, treatment with Aβ25-35 increased the expression levels of PGE2 and TNF-α, increased the activity of LDH, and up-regulated the mRNA and protein expression of COX-2, IL-1β, and TNFR1. Treatment with BBR down-regulated the expression levels of PGE2 and TNF-α, decreased the activity of LDH, and downregulated the mRNA and protein expression of COX-2, IL-1β, and TNFR1. Taken together, the present results suggested that BBR suppressed the inflammatory response induced by Aβ25-35 in neuroblastoma cells. The mechanism of action may be associated with the inhibition of proinflammatory factors.
Keywords: amyloid β peptide; berberine; cyclooxygenase 2; inflammatory response; tumor necrosis factor-α.