ArticleJournal of molecular histology2022
Isoorientin suppresses sepsis-induced acute lung injury in mice by activating an EPCR-dependent JAK2/STAT3 pathway.
Article in Journal of molecular histology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Global research progress of endothelial cells and ALI/ARDS: a bibliometric analysis.Frontiers in physiology · 2024Pooled it
- Comparative analysis ofPharmaceutical biology · 2026Article
- Exploring the Mechanism of Bu Zhong Yi Qi Decoction in Treating Sepsis-induced Acute Lung Injury based on Network Pharmacology and Experimental Verification.Current pharmaceutical design · 2026Article
- Oroxin B prevented sepsis-evoked acute lung injury by promoting M2 macrophage polarization through the TLR4/NF-κB axis.Histology and histopathology · 2025Article
- Identification of active metabolites fromFrontiers in pharmacology · 2025Article
- Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications.Cell communication and signaling : CCS · 2024Review
- Mechanisms of Sepsis-Induced Acute Lung Injury and Advancements of Natural Small Molecules in Its Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Protective effect and mechanism of Sufentanil on acute lung injury in septic mice.Frontiers in pharmacology · 2024Article
- From Basic Research to Clinical Practice: Considerations for Treatment Drugs for Silicosis.International journal of molecular sciences · 2023Review
- Tocilizumab attenuates acute lung injury in rats with sepsis by regulating S100A12/NLRP3.American journal of translational research · 2023Article
- Anti-Inflammatory Effects of Phytochemical Components ofMolecules (Basel, Switzerland) · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a systemic inflammatory syndrome, and acute lung injury (ALI) is one of the most common fatal complications of sepsis. Isoorientin (ISO) exerts a momentous role in the regulation of inflammation. However, whether ISO has a protective effect on sepsis-induced ALI remains unknown. This research aimed to elucidate the function of ISO on sepsis-induced ALI and its mechanism. In this study, the sepsis-induced ALI was established in the male C57BL/6 J mice. Functionally, ISO reduced the total protein concentration in BALF, lung wet/dry ratio and the numbers of neutrophils and macrophages in BALF as well as ameliorated lung injury. Besides, ISO treatment decreased the cytokine expressions and oxidative stress, and repressed the adhesion and migration of inflammatory cells induced by CLP. Mechanistically, ISO reduced the shedding of EPCR in the endothelial cell membrane; ISO treatment activated the JAK2/STAT3 signaling pathway through EPCR and the JAK2/STAT3 pathway inhibitors repressed the anti-inflammatory and antioxidant effects of ISO. In general, ISO suppressed sepsis-induced ALI in mice by activating an EPCR-dependent JAK2/STAT3 pathway.
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