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 β-amyloid peptides 25-35 (Aβ25-35). Accordingly, we evaluated the inflammatory damage induced by Aβ25-35 and the protective effect of GEN against Aβ25-35 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 Aβ25-35 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)-α and interleukin (IL)-1β 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 (IκB-α). The current results showed that GEN could alleviate Aβ25-35-induced cell apoptosis and prevent Aβ25-35-induced TNF-α and IL-1β release from C6 cells. In addition, GEN prevented Aβ25-35-induced upregulation of the gene and protein expression of TLR4, and GEN significantly upregulated the expression of IκB-α in C6 cells damaged by Aβ25-35. These results suggest that GEN can alleviate the inflammatory stress caused by Aβ25-35 treatment, which might be associated with the neuroprotective effect of GEN regulating the TLR4/NFκB signaling pathway.
School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University , Beijing, People's Republic of China .
Weiwei
W
Ma
Bingjie
B
Ding
Huanling
H
Yu
Linhong
L
Yuan
Yuandi
Y
Xi
Rong
R
Xiao
D016229:Amyloid beta-Peptides / Q000009:adverse effects / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D002460:Cell Line; D015870:Gene Expression / Q000187:drug effects; D019833:Genistein / Q000494:pharmacology / Q000627:therapeutic use*; D020672:I-kappa B Proteins / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D010446:Peptide Fragments / Q000009:adverse effects / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D015398:Signal Transduction; D013025:Glycine max / Q000737:chemistry*; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D015854:Up-Regulation
D016229:Amyloid beta-Peptides; D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D018696:Neuroprotective Agents; C000606206:Nfkbia protein, rat; D010446:Peptide Fragments; D010936:Plant Extracts; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; C074636:amyloid beta-protein (25-35); D000072000:NF-KappaB Inhibitor alpha; D019833:Genistein
beta-amyloid peptides; genistein; inflammatory factors; neuroprotection