Genistein Alleviates β-Amyloid-Induced Inflammatory Damage Through Regulating Toll-Like Receptor 4/Nuclear Factor κB

Genistein (GEN), a major soybean isoflavone (SIF), might possess neuroprotective properties through its anti-inflammatory activity. We hypothesized that GEN could prevent the inflammatory damage detected in C6 cells induced by beta-amyloid peptides 25-35 (A beta 25-35). Accordingly, we evaluated the inflammatory damage induced by A beta 25-35 and the protective effect of GEN against A beta 25-35 in C6 cells. In our study, the C6 glial cells (rats glioma cell lines) were preincubated with or without GEN for 2 h following incubation with A beta 25-35 for another 24 h. Then, methylthiazolyl tetrazolium (MTT) assay was used to assess the cell viability. Immunofluorescence staining was used to identify the C6 cells. Inflammatory factors tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta were analyzed by using enzyme-linked immunosorbent assay (ELISA). Western blot analysis and reverse transcription-polymerase chain reaction analysis were performed to assess the expression of Toll-like receptors 4 (TLR4), inhibitor of kappaB-alpha (I kappa B-alpha). The current results showed that GEN could alleviate A beta 25-35-induced cell apoptosis and prevent A beta 25-35-induced TNF-alpha and IL-1 beta release from C6 cells. In addition, GEN prevented A beta 25-35-induced upregulation of the gene and protein expression of TLR4, and GEN significantly upregulated the expression of I kappa B-alpha in C6 cells damaged by A beta 25-35. These results suggest that GEN can alleviate the inflammatory stress caused by A beta 25-35 treatment, which might be associated with the neuroprotective effect of GEN regulating the TLR4/NF kappa B signaling pathway.