Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
[Sulforaphane reverses Aβ fiber-mediated M1 type microglia polarization and neuroinflammation-mediated necroptosis of neural stem cells by downregulating the MAPK/NF-κB signaling pathways].
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Zhang J, Yang C, Zhang S, Cao T, Peng R, Guo W, Yan Y, Xie S, Peng X, Lü T, Huang T
Аннотация
OBJECTIVE: To explore the effects of sulforaphane (SFN) and Aβ25-35 fibers (fAβ25-35) on M1/M2 polarization of BV-2 cells and neuroinflammation-mediated programmed necrosis of neural stem cells.
METHODS: BV-2 cells treated with different concentrations of fAβ25-35 and SFN were examined for changes in cell viability using the CCK-8 kit. The effect of fAβ25-35 alone or in combination with SFN or SB203580 on expressions of IL-6 and TNF-α mRNA and proteins were assessed in BV-2 cells using RT-qPCR and ELISA. CD16/32 and CD206 in the treated cells were analyzed with flow cytometry, and the cellular expressions of p-p38 and p-p65 protein were detected with Western blotting. C17.2 cells co-cultured with BV-2 cells for 24 h were examined for p-mlkl protein expression using Western blotting.
RESULTS: fAβ25-35 at the concentration of 6.25 μmol/L significantly increased the viability of BV-2 cells (P < 0.01) whereas fAβ25-35 beyond 50 μmol/L decreased the cell viability (P < 0.0001). Treatment of BV-2 cells with SFN below 10 μmol/L for 24 h did not significant affect the cell viability (P > 0.05). BV-2 cells treated with fAβ25-35 alone, as compared with the cells in the other 3 groups, showed significantly increased IL-6 and TNF-α mRNA and protein expressions (P < 0.001), enhanced CD16/32 expression (P < 0.05), lowered CD206 expression (P < 0.01), and increased protein expressions of p-p38 and p- p65 (P < 0.01). C17.2 cells co-cultured with BV-2 cells treated with fAβ25-35, compared with the combined treatments, showed a significant reduction in the protein expression of p-mlkl (P < 0.05).
CONCLUSION: SFN reverses M1 type microglia polarization and neuroinflammation-mediated programmed necrosis of neural stem cells by downregulating the MAPK/NF-κB signaling pathway in Aβ25-35-activated BV-2 cells.
METHODS: BV-2 cells treated with different concentrations of fAβ25-35 and SFN were examined for changes in cell viability using the CCK-8 kit. The effect of fAβ25-35 alone or in combination with SFN or SB203580 on expressions of IL-6 and TNF-α mRNA and proteins were assessed in BV-2 cells using RT-qPCR and ELISA. CD16/32 and CD206 in the treated cells were analyzed with flow cytometry, and the cellular expressions of p-p38 and p-p65 protein were detected with Western blotting. C17.2 cells co-cultured with BV-2 cells for 24 h were examined for p-mlkl protein expression using Western blotting.
RESULTS: fAβ25-35 at the concentration of 6.25 μmol/L significantly increased the viability of BV-2 cells (P < 0.01) whereas fAβ25-35 beyond 50 μmol/L decreased the cell viability (P < 0.0001). Treatment of BV-2 cells with SFN below 10 μmol/L for 24 h did not significant affect the cell viability (P > 0.05). BV-2 cells treated with fAβ25-35 alone, as compared with the cells in the other 3 groups, showed significantly increased IL-6 and TNF-α mRNA and protein expressions (P < 0.001), enhanced CD16/32 expression (P < 0.05), lowered CD206 expression (P < 0.01), and increased protein expressions of p-p38 and p- p65 (P < 0.01). C17.2 cells co-cultured with BV-2 cells treated with fAβ25-35, compared with the combined treatments, showed a significant reduction in the protein expression of p-mlkl (P < 0.05).
CONCLUSION: SFN reverses M1 type microglia polarization and neuroinflammation-mediated programmed necrosis of neural stem cells by downregulating the MAPK/NF-κB signaling pathway in Aβ25-35-activated BV-2 cells.