Genistein inhibited amyloid-β induced inflammatory damage in C6 glial cells.
OBJECTIVE
β-amyloid-induced inflammation has been implicated in the early pathologic events in neurodegenerative diseases. The anti-inflammation potential of genistein (GEN) had been proved recently in our previous studies. We undertook this study to investigate the effects of GEN on inflammation induced by β-amyloid25-35 treatment and the possible molecular mechanisms in C6 glial cells.


METHODS
C6 cells were pre-incubated with GEN for 2 h followed by the incubation with β-amyloid 25-35 (Aβ25-35) for another 24 h. Inflammatory factors were detected by ELISA. The mRNA and protein expression of nuclear factor κB (NF-κB) p65 was measured using RT-PCR and Western blot, respectively. After inhibiting the NF-κBp65 mRNA expression by using short interfering RNAs (siRNAs) technique, the changes of inflammatory factors levels were detected again.


RESULTS
GEN inhibited the production of inflammatory factors induced by Aβ25-35 treatment. Aβ25-35 treatment had no effect on the mRNA expression of NF-κBp65 but upregulated the protein expression of NF-κBp65. However, this upregulation effect on NF-κBp65 protein expression was alleviated by GEN pretreatment. After inhibiting NF-κBp65 mRNA expression by using siRNA technique, the effects of Aβ25-35 or GEN on the inflammatory factor generation were inhibited.


CONCLUSIONS
These results indicated that GEN exhibited anti-inflammatory effects through regulating NF-κB signaling pathway in Aβ25-35-treated C6 glial cells.
School of Public Health, Capital Medical University, Beijing, PR China.
Xia
X
Zhao
School of Public Health, Capital Medical University, Beijing, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
Linhong
L
Yuan
School of Public Health, Capital Medical University, Beijing, PR China.
Huanling
H
Yu
School of Public Health, Capital Medical University, Beijing, PR China.
Yuandi
Y
Xi
School of Public Health, Capital Medical University, Beijing, PR China.
Weiwei
W
Ma
School of Public Health, Capital Medical University, Beijing, PR China.
Xin
X
Zhou
School of Public Health, Capital Medical University, Beijing, PR China.
Juan
J
Ding
School of Public Health, Capital Medical University, Beijing, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China. Electronic address: xiaor22@ccmu.edu.cn.
Rong
R
Xiao
D016229:Amyloid beta-Peptides / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D019833:Genistein / Q000494:pharmacology*; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D009457:Neuroglia / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010446:Peptide Fragments / Q000378:metabolism* / Q000633:toxicity; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D051381:Rats; D015398:Signal Transduction; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism
D016229:Amyloid beta-Peptides; D000893:Anti-Inflammatory Agents; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D051996:Transcription Factor RelA; C074636:amyloid beta-protein (25-35); D019833:Genistein
Genistein; Inflammatory damage; NF-κB; siRNA; β-amyloid peptides