ArticleJournal of molecular neuroscience : MN2020
Amitriptyline Reduces Sepsis-Induced Brain Damage Through TrkA Signaling Pathway.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
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- Senkyunolide I Improves Septicemia-Induced Brain Dysfunction via Regulating Nrf2 and Astrocyte Activity.Biotechnology and applied biochemistry · 2025Article
- Exploring Neuroprotective Agents for Sepsis-Associated Encephalopathy: A Comprehensive Review.International journal of molecular sciences · 2023Review
- HSF1 Alleviates Brain Injury by Inhibiting NLRP3-Induced Pyroptosis in a Sepsis Model.Mediators of inflammation · 2023Article
- Amitriptyline-Based Biodegradable PEG-PLGA Self-Assembled Nanoparticles Accelerate Cutaneous Wound Healing in Diabetic Rats.Pharmaceutics · 2022Article
- Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment.Oxidative medicine and cellular longevity · 2022Review
- Impact of history of mental disorders on short-term mortality among hospitalized patients with sepsis: A population-based cohort study.PloS one · 2022Article
- The regulatory role of the BDNF/TrkB pathway in organ and tissue fibrosis.Histology and histopathology · 2021Review
- Nerve growth factor enhances the therapeutic effect of mesenchymal stem cells on diabetic periodontitis.Experimental and therapeutic medicine · 2021Article
- Role of microRNAs As Biomarkers in Sepsis-Associated Encephalopathy.Molecular neurobiology · 2021Review
- Update on Functional Inhibitors of Acid Sphingomyelinase (FIASMAs) in SARS-CoV-2 Infection.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Association between Functional Inhibitors of Acid Sphingomyelinase (FIASMAs) and Reduced Risk of Death in COVID-19 Patients: A Retrospective Cohort Study.Pharmaceuticals (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis can induce acute and chronic changes in the central nervous system termed sepsis-associated encephalopathy (SAE). Not only cognitive deficits but also anxiety, depression, and post-traumatic stress disorder are common in severe sepsis survivors. In this study, we demonstrated that amitriptyline, a classic tricyclic antidepressant, reduced sepsis-induced brain damage through the tropomyosin receptor kinase A (TrkA) signaling pathway. Amitriptyline ameliorated neuronal loss assessed by Nissl staining in a mouse cecal ligation and puncture (CLP)-induced sepsis model. Furthermore, amitriptyline reduced early gliosis assessed by immunofluorescence and late cognitive deficits assessed by the Morris water maze (MWM) test. Moreover, amitriptyline treatment attenuated oxidative stress indicated by less superoxide dismutase (SOD) and catalase (CAT) activity consumption and malondialdehyde (MDA) accumulation. Interestingly, those protective effects of amitriptyline could be abolished by GW441756, a TrkA signaling pathway inhibitor. Immunoblot directly showed that TrkA signaling pathway-associated proteins, such as Akt and GSK3β, were involved in the neuroprotective effects of amitriptyline. Thus, amitriptyline appears to be an encouraging candidate to treat cognitive deficits and depression after severe sepsis.
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