ArticleHistology and histopathology2024
Functional mechanism of baicalein in alleviating severe acute pancreatitis-acute lung injury by blocking the TLR4/MyD88/TRIF signaling pathway.
Article in Histology and histopathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Molecular Mechanisms and Therapeutic Potential of Baicalein in Acute Pancreatitis: A Comprehensive Review.Biomolecules · 2026Review
- The mechanisms underlying COVID-19 induced insulin resistance: a narrative review.Frontiers in endocrinology · 2026Review
- SARS-CoV-2 Spike Protein as a Target of the COVID-19 Vaccine Disrupts Insulin Signaling in Type 2 Diabetes.MedComm · 2025Article
- An overview of current research on the modulation of NLRP3 inflammasome by traditional Chinese medicine to combat acute pancreatitis.Frontiers in molecular biosciences · 2025Review
- Identification of novel amino acid variants in the Han Chinese population that impair toll-like receptor 4 signaling and confer hyporesponsiveness to lipopolysaccharide.Frontiers in immunology · 2025Article
- Natural Compounds for the Treatment of Acute Pancreatitis: Novel Anti-Inflammatory Therapies.Biomolecules · 2024Review
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Severe acute pancreatitis-acute lung injury (SAP-ALI) is a disease with high mortality. This study aims to explore the mechanism of baicalein on SAP-ALI in rats by blocking toll-like receptor-4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88)/TIR-domain-containing adapter-inducing interferon-β (TRIF) signal pathway. The SAP-ALI rat model was established by intraperitoneal injection of 3% pentobarbital sodium (30 mg/kg), with pancreas and intestines turned over, injected with 3.5% sodium taurocholate backward into the bile-pancreatic duct at 0.1 mL/100 g for 12h, and treated with baicalein, lipopolysaccharide (LPS), miR-182 agomir, or miR-182 antagomir. The TLR4/MyD88/TRIF pathway was activated using LPS in SAP-ALI rats after baicalein treatment. Baicalein attenuated inflammatory cell infiltration, alveolar wall edema, decreased W/D ratio and levels of TLR4, MyD88, and TRIF in the lung tissues, reduced levels of inflammatory factors in pancreatic and lung tissues and BALF, diminished ROS, and elevated GSH, SOD and CAT in pancreatic and lung tissues of SAP-ALI rats. Activation of the TLR4/MyD88/TRIF pathway partly abrogated baicalein-mediated improvements in inflammation and oxidative stress in SAP-ALI rats. miR-182 targeted TLR4. miR-182 suppressed inflammation and oxidative stress in SAP-ALI rats by targeting TLR4. Inhibition of miR-182 partly nullified baicalein-mediated attenuation on inflammation and oxidative stress in SAP-ALI rats. In conclusion, baicalein can inhibit the TLR4/MyD88/TRIF pathway and alleviate inflammatory response and oxidative stress in SAP-ALI rats by upregulating miR-182 and suppressing TLR4, thus ameliorating SAP-ALI.
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