ArticlePloS one2025
The effect of lidocaine against sepsis-induced acute lung injury in a mouse model through the JAK2/STAT3 pathway.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Baihe Gujin decoction ameliorates sepsis-induced acute lung injury through Nrf2/GPX4-mediated antioxidant defense and PPARα-driven metabolic reprogramming: a multi-omics investigation.Frontiers in immunology · 2026Article
- Selective JAK2 inhibition by TG101209 reprograms macrophage polarization and alleviates acute lung injury.Frontiers in immunology · 2026Article
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to investigate the effects of lidocaine on sepsis-induced acute lung injury and its underlying mechanisms.
methodsThirty C57BL/6 mice were divided into three groups: SHAM, CLP, and LD. The sepsis-induced acute lung injury model was established using cecal ligation and puncture (CLP) surgery, while SHAM mice underwent a sham operation without ligation or puncture. Mice in the LD group were administered lidocaine (10 mg/kg) intravenously through the tail vein. The SHAM and CLP groups were treated with an equal volume of 0.9% sterile saline solution. All mice were sacrificed 24 hours after surgery, and lung tissue and blood samples were collected for subsequent analysis. The wet/dry weight ratio (W/D ratio) was measured to evaluate lung edema. Lung injury and apoptosis were assessed using HE staining and TUNEL assay. The concentrations of inflammatory cytokines IL-6, TNF-α, and HMGB1 were measured by ELISA. The expression of JAK2, STAT3, p-STAT3, Bcl-2, HMGB1, and Bax was analyzed by western blot.
resultsThe W/D ratio in the CLP group was significantly higher than the SHAM group, indicating increased lung edema. Pathological examination revealed obvious lung injury, and apoptosis was evident in the CLP group. The expression of HMGB1, IL-6, and TNF-α in lung tissue increased by 24 hours after CLP surgery. Additionally, the levels of JAK2, STAT3, p-STAT3, HMGB1, and Bax were significantly increased, while Bcl-2 expression was reduced. However, lidocaine administration reversed these changes.
conclusionIntravenous lidocaine effectively alleviated acute lung injury in septic mice. The anti-inflammatory effects of lidocaine may be attributed to its suppression of the JAK2/STAT3 signaling pathway and its anti-apoptotic effects.
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