Oxidized black carbon induced inflammatory responses and associated mechanisms in SH-SY5Y cells
Human neuroblastoma cell SH-SY5Y was applied as a cell line model in order to explore its inflammatory responses to ozone oxidized black carbon(OBC)and also to investigate the potential roles of the nuclear factor-KB(NF-κB)and phosphatidylin-ositol-3-kinase/protein kinase B(PI3K/Akt)pathways.The results showed that mitochondrial membrane potential(MMP)decreased and the degree of DNA damage increased signifi-cantly in a time-and concentration-dependent manner in SH-SY5Y cells after treatment with OBC.Interleukin-4(IL-4)leakage and the expression of tumor necrosis factor-α(TNF-α)mRNA were found to increase concentration-dependently,suggesting that OBC could lead to inflammatory responses in SH-SY5Y cells.Meanwhile,significantly elevated in-tracellular reactive oxygen species(ROS)levels and the mRNA expression of superoxide dismutase(SOD)and heme oxygenase-1(HO-1)demonstrated that OBC caused oxidative stress in SH-SY5Y cells.OBC activated the NF-κB and PI3K/Akt pathways,indicated by significant changes seen in certain proteins.In summary,the NF-κB and PI3K/Akt pathways probably played important roles in OBC promoted oxidative stress and the in-flammatory responses seen in SH-SY5Y cells.
black carbon(BC)SH-SY5Y cellsinflammatory responsesnuclear factor-KB(NF-κB)
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