ArticleBehavioural neurology2022
The Improvement of Sepsis-Associated Encephalopathy by P2X7R Inhibitor through Inhibiting the Omi/HtrA2 Apoptotic Signaling Pathway.
Article in Behavioural neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- The Participation of Acetyl Phosphate, a Microbial and Host Metabolite, in the Regulation of the Calcium Balance in Mitochondria and Cells.International journal of molecular sciences · 2026Article
- P2X7 receptor: a potential therapeutic target for chronic respiratory diseases.Molecular and cellular biochemistry · 2026Review
- Mitochondrial dysfunction, neuroinflammation, and associated mechanisms in sepsis-associated encephalopathy: from pathogenesis to emerging therapeutics.Frontiers in neuroscience · 2026Review
- Mesenchymal stem cells in sepsis-induced organ dysfunction: mechanisms and therapeutic potential.Stem cell research & therapy · 2025Review
- Blood‑brain barrier dysfunction in epilepsy: Mechanisms, therapeutic strategies and future orientation (Review).International journal of molecular medicine · 2025Review
- Photoacoustic imaging detects cerebrovascular pathological changes in sepsis.Photoacoustics · 2025Article
- Role of PScientific reports · 2025Article
- High-temperature requirement serine protease A2 inhibitor UCF-101 ameliorates damaged neurons in traumatic brain-injured rats by the AMPK/NF-κB pathway.Open life sciences · 2025Article
- Exploring the Therapeutic Potential of Baicalin: Mitigating Anxiety and Depression in Epileptic Rats.Combinatorial chemistry & high throughput screening · 2025Article
- Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy.Frontiers in pharmacology · 2025Article
- Propofol and Dexmedetomidine Ameliorate Endotoxemia-Associated Encephalopathy via Inhibiting Ferroptosis.Drug design, development and therapy · 2024Article
- P2X7 receptor: A receptor closely linked with sepsis-associated encephalopathy.Open life sciences · 2024Review
- The Absence of Gasdermin D Reduces Nuclear Autophagy in a Cecal Ligation and Puncture-Induced Sepsis-Associated Encephalopathy Mouse Model.Brain sciences · 2023Article
- Purinergic signaling: A gatekeeper of blood-brain barrier permeation.Frontiers in pharmacology · 2023Review
- P2X7 receptor contributes to long-term neuroinflammation and cognitive impairment in sepsis-surviving mice.Frontiers in pharmacology · 2023Article
- Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of sepsis-associated encephalopathy (SAE) involves many aspects, including intracellular peroxidative stress damage, mitochondrial dysfunction, and cell apoptosis. In this study, we mainly explored the influence of P2X7R on the cognitive function of SAE and its molecular mechanism. We established a sepsis model using lipopolysaccharide (LPS) stimulation, followed by an assessment of cognitive function using Morris water maze, and then Western Blot was used to analyze the expression of tight junction proteins ZO-1 and Occludin in the hippocampus of mice. TUNEL assay was used to analyze the apoptosis of brain cells in frozen brain slices of mice during sepsis. Human brain microvascular endothelial cells (HBMECs) were used to research the molecular mechanism of brain cell damage induced by P2X7R. The results showed that P2X7R inhibitors dramatically improved the survival rate of mice, relieved the cognitive dysfunction caused by LPS stimulation, and significantly reduced the brain cell apoptosis caused by LPS. In addition, the inhibition of P2X7R can also reduce the production and accumulation of reactive oxygen species (ROS) in HBMECs in vitro and inhibit the apoptosis signaling pathway associated with mitochondrial serine protease Omi/HtrA2 in HBMECs in vitro. These results suggest that P2X7R has strong value as a potential target for the treatment of SAE.
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