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Fig. 6 | Molecular Medicine

Fig. 6

From: Involvement of Fgf2-mediated tau protein phosphorylation in cognitive deficits induced by sevoflurane in aged rats

Fig. 6

Fgf2 promotes abnormal accumulation of tau protein and neurofibrillary tangle formation by regulating Gsk3b. Note: (A) Western blot analysis of PI3K, P-PI3K, AKT, P-AKT, Gsk3b, P-Gsk3b, tau, and P-tau protein expression in Sevo model rats. (B) Statistical analysis of P-PI3K/PI3K and P-AKT/AKT protein expression ratios. (C) Statistical analysis of P-Gsk3b/Gsk3b and P-tau/tau protein expression ratios. (D) Immunohistochemistry and corresponding quantitative analysis of Fgf2 in the CA3 and CA1 regions confirmed the successful knockdown of Fgf2 in the CA3 region. (E) Immunofluorescence detection of P-tau content in hippocampal tissues of Sevo model rats. (F) Immunofluorescence detection of neurofibrillary tangles in hippocampal tissues of Sevo model rats. Sevo group compared to Control group, **P < 0.01; ## indicates comparison between Sevo + sh-Fgf2 + DMSO or Sevo + sh-Fgf2 + act-Gsk3b group to the Sevo + sh-NC + DMSO groups, P < 0.01; & indicates comparison between Sevo + sh-Fgf2 + act-Gsk3b and Sevo + sh-Fgf2 + DMSO groups, P < 0.05. Each treatment group consisted of seven rats, and all experiments were repeated three times

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