Xia Zhao1, Linhong Yuan2, Huanling Yu1, Yuandi Xi1, Weiwei Ma1, Xin Zhou1, Juan Ding1, Rong Xiao3. 1. School of Public Health, Capital Medical University, Beijing, PR China. 2. School of Public Health, Capital Medical University, Beijing, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China. 3. 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.
Abstract
BACKGROUND AND AIMS: 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.
BACKGROUND AND AIMS: 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.