ArticleJournal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban2016
Telmisartan reduced cerebral edema by inhibiting NLRP3 inflammasome in mice with cold brain injury.
Article in Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Inflammasomes in glioblastoma.Journal of neuroinflammation · 2026Review
- Loss of AMPK potentiates inflammation by activating the infammasome in a preclinical mouse model of TBI.NeuroImmune pharmacology and therapeutics · 2026Article
- The application of telmisartan in central nervous system disorders.Pharmacological reports : PR · 2025Review
- Detection of NLRP3, ASC, and Caspase-1 in serum and cerebrospinal fluid of traumatic brain injury patients: implications for short-term prognosis.Acta neurologica Belgica · 2025Article
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- Inflammasomes at the crossroads of traumatic brain injury and post-traumatic epilepsy.Journal of neuroinflammation · 2024Review
- Voluntary Exercise to Reduce Anxiety Behaviour in Traumatic Brain Injury Shown to Alleviate Inflammatory Brain Response in Mice.International journal of molecular sciences · 2023Article
- Inflammasomes as biomarkers and therapeutic targets in traumatic brain injury and related-neurodegenerative diseases: A comprehensive overview.Neuroscience and biobehavioral reviews · 2023Review
- Compound 21, a Direct AT2R Agonist, Induces IL-10 and Inhibits Inflammation in Mice Following Traumatic Brain Injury.Neuromolecular medicine · 2022Article
- Mesenchymal stem cells protect against TBI-induced pyroptosis in vivo and in vitro through TSG-6.Cell communication and signaling : CCS · 2022Article
- Telmisartan attenuates human glioblastoma cells proliferation and oncogenicity by inducing the lipid oxidation.Asia-Pacific journal of clinical oncology · 2022Article
- TI: NLRP3 Inflammasome-Dependent Pyroptosis in CNS Trauma: A Potential Therapeutic Target.Frontiers in cell and developmental biology · 2022Review
- Neuroprotective and Anti-inflammatory Effects of Pioglitazone on Traumatic Brain Injury.Mediators of inflammation · 2022Review
- The NLRP3 inflammasome: a potential therapeutic target for traumatic brain injury.Neural regeneration research · 2021Article
- Candesartan could ameliorate the COVID-19 cytokine storm.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Article
- The Role of NLRP3 Inflammasome in the Pathogenesis of Traumatic Brain Injury.International journal of molecular sciences · 2020Review
- The NLRP3 inflammasome in traumatic brain injury: potential as a biomarker and therapeutic target.Journal of neuroinflammation · 2020Review
- Neuroinflammation and blood-brain barrier disruption following traumatic brain injury: Pathophysiology and potential therapeutic targets.Journal of neuroscience research · 2020Review
- NLRs as Helpline in the Brain: Mechanisms and Therapeutic Implications.Molecular neurobiology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the possible beneficial role of telmisartan in cerebral edema after traumatic brain injury (TBI) and the potential mechanisms related to the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) pyrin domain-containing 3 (NLRP3) inflammasome activation. TBI model was established by cold-induced brain injury. Male C57BL/6 mice were randomly assigned into 3, 6, 12, 24, 48 and 72 h survival groups to investigate cerebral edema development with time and received 0, 5, 10, 20 and 40 mg/kg telmisartan by oral gavage, 1 h prior to TBI to determine the efficient anti-edemic dose. The therapeutic window was identified by post-treating 30 min, 1 h, 2 h and 4 h after TBI. Blood-brain barrier (BBB) integrity, the neurological function and histological injury were assessed, at the same time, the mRNA and protein expression levels of NLRP3 inflammasome, IL-1β and IL-18 concentrations in peri-contused brain tissue were measured 24 h post TBI. The results showed that the traumatic cerebral edema occurred from 6 h, reached the peak at 24 h and recovered to the baseline 72 h after TBI. A single oral dose of 5, 10 and 20 mg/kg telmisartan could reduce cerebral edema. Post-treatment up to 2 h effectively limited the edema development. Furthermore, prophylactic administration of telmisartan markedly inhibited BBB impairment, NLRP3, apoptotic speck-containing protein (ASC) and Caspase-1 activation, as well as IL-1β and IL-18 maturation, subsequently improved the neurological outcomes. In conclusion, telmisartan can reduce traumatic cerebral edema by inhibiting the NLRP3 inflammasome-regulated IL-1β and IL-18 accumulation.
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