ArticleMolecular medicine reports2019
Rapamycin improves sevoflurane‑induced cognitive dysfunction in aged rats by mediating autophagy through the TLR4/MyD88/NF‑κB signaling pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Morroniside ameliorates sevoflurane anesthesia-induced cognitive dysfunction in aged mice through modulating the TLR4/NF-κB pathway.Biomolecules & biomedicine · 2025Article
- Review
- Environmental enrichment attenuates sevoflurane anesthesia-induced learning deficits in aged mice through regulating TTBK1 and phosphorylated Tau expression.Experimental brain research · 2025Article
- CircUBE3B High Expression Participates in Sevoflurane-Induced Human Hippocampal Neuron Injury via Targeting miR-326 and Regulating MYD88 Expression.Neurotoxicity research · 2023Article
- Exogenous recombinant Hsp70 attenuates sevoflurane anesthesia-induced cognitive dysfunction in aged mice.Brain and behavior · 2023Article
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- Polyvinylpyrrolidone-Modified Taxifolin Liposomes Promote Liver Repair by Modulating Autophagy to Inhibit Activation of the TLR4/NF-κB Signaling Pathway.Frontiers in bioengineering and biotechnology · 2022Article
- Inhibition of Adult Hippocampal Neurogenesis Plays a Role in Sevoflurane-Induced Cognitive Impairment in Aged Mice Through Brain-Derived Neurotrophic Factor/Tyrosine Receptor Kinase B and Neurotrophin-3/Tropomyosin Receptor Kinase C Pathways.Frontiers in aging neuroscience · 2022Article
- Key miRNAs associated with memory and learning disorder upon exposure to sevoflurane determined by RNA sequencing.Molecular medicine reports · 2020Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was aimed to observe the protective effect of rapamycin on cognitive dysfunction induced by sevoflurane in aged rats and its effect on autophagy‑related proteins, and to investigate the regulatory mechanism of the Toll‑like receptor 4/myeloid differentiation primary response 88/nuclear factor‑κB (TLR4/MyD88/NF‑κB) signaling pathway. Fifty Sprague‑Dawley rats were randomly assigned to a control group, a sevoflurane group, a rapamycin pretreatment group, a TLR4 inhibitor group and a 3MA autophagy inhibitor group. A water maze test was used to evaluate the cognition and memory of rats. Hematoxylin and eosin (H&E) staining was performed to observe pathological changes of brain tissue. A TUNEL assay was used to detect the apoptosis of brain tissue. ELISA was used to assess changes in brain injury markers and inflammatory factors. A western blot assay or quantitative reverse transcription PCR (RT‑qPCR) were performed to determine the expression of autophagy‑related proteins and the TLR4/MyD88/NF‑κB signaling pathway in brain tissue. The results revealed that rapamycin could improve cognitive dysfunction of aged rats induced by sevoflurane. Rapamycin was identified to play a therapeutic role, including mitigating brain tissue damage, inhibiting apoptosis, and activating autophagy in a sevoflurane‑treated aged rat model. This function of rapamycin was demonstrated to depend on the TLR4/MyD88/NF‑κB signaling pathway.
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