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. 2019 Jul 31;20(4):3085–3094. doi: 10.3892/mmr.2019.10541

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Copyright: © Li et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 6. — Rapamycin improves sevoflurane-induced cognitive dysfunction in aged rats by mediating autophagy through the TLR4/MyD88/NF-κB signaling pathway. (A) Western blot assays were performed to determine the protein expression levels of LC3II/I, Beclin1 and p62 proteins. (B) ELISA was performed to determine the expression levels of IL-1β, IL-6, TNF-α and IL-10. (C) An MWM experiment was conducted to determine the effects of the TLR4/MyD88/NF-κB signaling pathway on learning and memory abilities. *P<0.05 vs. the RAP group. TLR4, toll-like receptor 4; MyD88, myeloid differentiation primary response 88; NF-κB, nuclear factor-κB; MWM, Morris water maze; TLR, TLR4 inhibitor.