Dl-3-n-Butylphthalide Improves Neuroinflammation in Mice with Repeated Cerebral Ischemia-Reperfusion Injury through the Nrf2-Mediated Antioxidant Response and TLR4/MyD88/NF-κB Signaling Pathway

Figure 8

NBP alleviated RCIR-induced inflammatory response, but with reduced inhibitory role in Nrf2^-/- mice. (a)–(c) ELISA analysis showing the expression of the inflammatory factors TNF-α, IL-6, and IL-1β in the hippocampus of WT and Nrf2^-/- mice 4 weeks after RCIR. per group. (d)–(g) Western blot analysis showing the expression of TLR4, MyD88, and p-NF-κB in WT and Nrf2^-/- mice at 4 weeks after RCIR. per group. β-Actin was used as an internal control. (h) Representative immunofluorescent micrographs of the hippocampus after staining with NF-κB primary antibody in WT and Nrf2^-/- mice 4 weeks after RCIR injury. Green fluorescence, NF-κB-positive cells; white arrow, nuclear translocation of NF-κB after RCIR with or without NBP treatment. . in each group. ^#, ^##, ^###, the vs. the group; ns: not significant, as indicated. Values are expressed as .

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