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 6

NBP failed to promote nuclear-Nrf2 accumulation and mitigate oxidative stress injury in Nrf2 knockout (Nrf2^-/-) mice. (a) The results of genotype identification by PCR. (b)–(d) NBP treatment failed to alleviate the activity of SOD, the content of MDA, and the level of 8-iso PGF2α in Nrf2^-/- mice after RCIR injury. or 10 per group. (e)–(h) Nuclear-Nrf2, HO-1, and NQO1 expressions were detected by Western blot in WT and Nrf2^-/- mice 4 weeks after RCIR. NBP treatment failed to upregulate the nuclear-Nrf2, HO-1, and NQO1 expressions in Nrf2^-/- mice compared to the WT group. per group. β-Actin was used as an internal control. (i) The effect of NBP on Nrf2 nuclear accumulation was determined by immunofluorescent (400×, ) in WT and Nrf2^-/- mice 4 weeks after RCIR. in each group. ^#, ^###, the vs. the WT+ RCIR group; ^&, ^&&&, the group vs. the group; ns: not significant, as indicated. Values are expressed as .

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