ArticleOxidative medicine and cellular longevity2021
Lidocaine Alleviates Sepsis-Induced Acute Lung Injury in Mice by Suppressing Tissue Factor and Matrix Metalloproteinase-2/9.
Article in Oxidative medicine and cellular longevity, 2021. 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, 21 citations in OpenAlex.
- Immunomodulatory Effects of Lidocaine: Mechanisms of Actions and Therapeutic Applications.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Tissue factor detection in mouse tissues by western blotting using commercial antibodies.Research and practice in thrombosis and haemostasis · 2026Article
- Article
- IsLife (Basel, Switzerland) · 2025Article
- RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025Review
- Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications.Cell communication and signaling : CCS · 2024Review
- Proteolytic Vesicles Derived fromBiomedicines · 2024Article
- PAMPs and DAMPs in Sepsis: A Review of Their Molecular Features and Potential Clinical Implications.International journal of molecular sciences · 2024Review
- Lidocaine pretreatment attenuates inflammatory response and protects against sepsis-induced acute lung injury via inhibiting potassium efflux-dependent NLRP3 activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Crosstalk between septic shock and venous thromboembolism: a bioinformatics and immunoassay analysis.Frontiers in cellular and infection microbiology · 2023Article
- Endothelial dysfunction and immunothrombosis in sepsis.Frontiers in immunology · 2023Review
- Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is one of the fatal symptoms of sepsis. However, there were no effective clinical treatments. TF accumulation-induced fibrin deposit formations and coagulation abnormalities in pulmonary vessels contribute to the lethality of ALI. Suppressor of cytokine signaling 3 (SOCS3) acts as an endogenous negative regulator of the TLR4/TF pathway. We hypothesized that inducing SOCS3 expression using lidocaine to suppress the TLR4/TF pathway may alleviate ALI. Hematoxylin and eosin (H&E), B-mode ultrasound, and flow cytometry were used to measure the pathological damage of mice. Gelatin zymography was used to measure matrix metalloproteinase-2/9 (MMP-2/9) activities. Western blot was used to assay the expression of protein levels. Here, we show that lidocaine could increase the survival rate of ALI mice and ameliorate the lung injury of ALI mice including reducing the edema, neutrophil infiltration, and pulmonary thrombosis formation and increasing blood flow velocity. Moreover,
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.