The Protective Effects of Annexin A1 in Acute Lung Injury Mediated by Nrf2 DOI Creative Commons
Hui Huang, Yuqin Shi, Yuequan Zhou

et al.

Immunity Inflammation and Disease, Journal Year: 2025, Volume and Issue: 13(1)

Published: Jan. 1, 2025

Acute lung injury (ALI), one of the most severe respiratory system diseases, is prevalent worldwide. Annexin A1 (AnxA1) an important member annexin superfamily, known for its wide range physiological functions. However, potential protective effect against lipopolysaccharide (LPS)-induced ALI remains unclear. Mice were divided into four groups: Sham, LPS + vehicle, 0.1 μg AnxA1, and 0.5 AnxA1. Lung was assessed through histopathology, pulmonary wet-to-dry (W/D) ratio, cell counting bronchoalveolar lavage fluid (BALF), oxidative stress analysis, noninvasive function testing. Gene protein expression levels measured using RT-PCR, ELISA, western blot analysis. AnxA1 alleviated LPS-induced by protecting tissue from damage, reducing wet/dry weight improving impaired function. Interestingly, administration found to repress infiltration inflammatory cells decreasing total count, neutrophils, concentrations in (BALF). mitigated response lowering IL-1β, IL-6, TNF-α BALF mice. Additionally, attenuated tissues mice restoring activity catalase (CAT), SOD, glutathione (GSH) but malondialdehyde (MDA). We also that suppressed activation NLRP3 signaling pathway. Mechanistically, activated Nrf2/HO-1 pathway while preventing NF-κB. Collectively, these findings suggest alleviates might be a promising novel therapeutic agent ALI.

Language: Английский

Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications DOI Creative Commons

Xinyu Qiao,

Junhao Yin,

Zhihuan Zheng

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: April 25, 2024

Abstract Sepsis, a prevalent critical condition in clinics, continues to be the leading cause of death from infections and global healthcare issue. Among organs susceptible harmful effects sepsis, lungs are notably most frequently affected. Consequently, patients with sepsis predisposed developing acute lung injury (ALI), severe cases, respiratory distress syndrome (ARDS). Nevertheless, precise mechanisms associated onset ALI/ARDS remain elusive. In recent years, there has been growing emphasis on role endothelial cells (ECs), cell type integral barrier function, their interactions various stromal sepsis-induced ALI/ARDS. this comprehensive review, we summarize involvement intricate interplay immune cells, including pulmonary epithelial fibroblasts, pathogenesis ALI/ARDS, particular placed discussing several pivotal pathways implicated process. Furthermore, discuss potential therapeutic interventions for modulating functions relevant present strategy managing

Language: Английский

Citations

29

Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS) DOI Creative Commons
Qianrui Huang, Yue Le, Shusheng Li

et al.

Respiratory Research, Journal Year: 2024, Volume and Issue: 25(1)

Published: Jan. 13, 2024

Abstract Acute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With outbreak coronavirus disease 19 worldwide, has increased correspondingly. Comprehending pathophysiology underlying molecular mechanisms may thus be essential developing therapeutic strategies reducing mortality. To facilitate further understanding its pathogenesis exploring novel therapeutics, this review provides comprehensive information from presents therapeutics. We first describe that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance oxidative stress. Next, we summarize signaling pathways related above four aspects pathophysiology, along latest research progress. Finally, discuss emerging show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies mesenchymal stromal cell highlighting pathophysiological basis influences on signal transduction for their use.

Language: Английский

Citations

24

Anti-inflammatory effect of polysaccharides from Sambucus williamsii Hance roots in lipopolysaccharide-stimulated RAW264.7 macrophages and acute lung injury in mice DOI

Xianqun Meng,

Qing Wei, Siyi Wang

et al.

International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: 306, P. 141368 - 141368

Published: Feb. 21, 2025

Language: Английский

Citations

2

The Molecular Pharmacology of Phloretin: Anti-Inflammatory Mechanisms of Action DOI Creative Commons
Solomon Habtemariam

Biomedicines, Journal Year: 2023, Volume and Issue: 11(1), P. 143 - 143

Published: Jan. 6, 2023

The isolation of phlorizin from the bark an apple tree in 1835 led to a flurry research on its inhibitory effect glucose transporters intestine and kidney. Using as prototype drug, antidiabetic agents with more selective activity towards transport at kidney have subsequently been developed. In contrast, hydrolysis product body, phloretin, which is also found plant, has weak properties. Phloretin, however, displays range pharmacological effects including antibacterial, anticancer, cellular organ protective properties both vitro vivo. this communication, molecular basis anti-inflammatory mechanisms that attribute scrutinised. These include inhibiting signalling pathways inflammatory mediators' expression support suppressive immune cells overactivation, obesity-induced inflammation, arthritis, endothelial, myocardial, hepatic, renal lung injury, inflammation gut, skin, nervous system, among others.

Language: Английский

Citations

40

Mechanisms of Sepsis-Induced Acute Lung Injury and Advancements of Natural Small Molecules in Its Treatment DOI Creative Commons
Yaxi Xu,

Jianzeng Xin,

Yupei Sun

et al.

Pharmaceuticals, Journal Year: 2024, Volume and Issue: 17(4), P. 472 - 472

Published: April 8, 2024

Sepsis-induced acute lung injury (ALI), characterized by widespread dysfunction, is associated with significant morbidity and mortality due to the lack of effective pharmacological treatments available clinically. Small-molecule compounds derived from natural products represent an innovative source have demonstrated therapeutic potential against sepsis-induced ALI. These small molecules may provide a promising alternative treatment option for This review aims summarize pathogenesis sepsis targets. It assembles critical updates (from 2014 2024) on ALI, detailing their sources, structures, effects, mechanisms action.

Language: Английский

Citations

13

Exploring immune-related pathogenesis in lung injury: Providing new insights Into ALI/ARDS DOI Open Access

Jiajing Zheng,

Ying Li, Xianbin Kong

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 175, P. 116773 - 116773

Published: May 21, 2024

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represent a significant global burden of morbidity mortality, with being the primary cause death in affected patients. The pathogenesis injury, however, remains complex issue. In recent years, role immune system has attracted extensive attention worldwide. Despite advancements our understanding various subtypes, limitations persist both prevention treatment. This review investigates immunopathogenesis ALI/ARDS, aiming to elucidate pathological processes mediated by dendritic cells (DCs), natural killer (NK) cells, phagocytes, neutrophils. Furthermore, article expounds on critical contributions gut microbiota, inflammatory pathways, cytokine storms development ALI/ARDS.

Language: Английский

Citations

11

Stimulation, regulation, and inflammaging interventions of natural compounds on nuclear factor kappa B (NF-kB) pathway: a comprehensive review DOI

Gowtham Kannan,

Benedict Mathews Paul, Parimelazhagan Thangaraj

et al.

Inflammopharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 7, 2025

Language: Английский

Citations

1

Balancing inflammation: the specific roles of serum amyloid A proteins in sterile and infectious diseasese DOI Creative Commons
Tirthankar Mohanty, Katarina Miličević,

Henri Göthert

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 10, 2025

Serum Amyloid A (SAA) proteins are acute-phase reactants with critical roles in sterile and bacterial inflammation. Through vitro vivo experiments, we demonstrate that SAA amplify cytokine chemokine responses during inflammation enhance clearance infectious conditions. Mechanistically, augment NF-κB signaling, driving pro anti-inflammatory mediator production. SAA-/- mice carrying a deletion of the Saa1, Saa2, Saa3, Saa4 serum amyloid genes have better survival rates sepsis but more prone to than their SAA+/+ counterparts, emphasizing dual functionality immune regulation. Overexpression macrophages enhances NF-κB-mediated pro-inflammatory production infection. Together, our results show key modulators inflammation, distinct mechanisms tailored contexts.

Language: Английский

Citations

1

Neutrophil-derived heparin-binding protein increases endothelial permeability in acute lung injury by promoting TRIM21 and the ubiquitination of P65 DOI Creative Commons
Jian Zhang, Yong Cao,

Wenqi Shu

et al.

Cell Biology and Toxicology, Journal Year: 2025, Volume and Issue: 41(1)

Published: March 5, 2025

Acute lung injury (ALI), which poses a significant public health threat, is commonly caused by sepsis. ALI associated with permeability and glycolysis changes in pulmonary microvascular endothelial cells. Our study demonstrates that heparin-binding protein (HBP), released from neutrophils during sepsis, exacerbates glycolysis, thereby triggering ALI. Through coimmunoprecipitation mass spectrometry, TRIM21 was identified as HBP interaction partner. Notably, enhances the stability of inhibiting K48 ubiquitination. binds to promotes K63-linked ubiquitination P65, facilitating its nuclear translocation. regulates HPMEC manner dependent on P65 stabilizes interactions P65. Rescue experiments conducted vivo vitro demonstrate modulation predominantly mediated through TRIM21-P65 axis. results suggest targeting HBP/TRIM21/P65 axis novel therapeutic strategy ameliorate

Language: Английский

Citations

1

Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury DOI Creative Commons

Yao Shen,

Yingying He, Ying Pan

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: Aug. 5, 2024

Sepsis-induced acute lung injury (ALI) is a major cause of death among patients with sepsis in intensive care units. By analyzing model sepsis-induced ALI using lipopolysaccharide (LPS) and cecal ligation puncture (CLP), treatment methods strategies to protect against were discussed, which could provide an experimental basis for the clinical ALI. Recent studies have found that imbalance autophagy, ferroptosis, pyroptosis key mechanism triggers ALI, regulating these mechanisms can improve injuries caused by LPS or CLP. This article summarized reviewed regulatory networks their important roles process LPS/CLP-induced sepsis, discusses possible targeted drugs above effects, describes dilemma prospects, provides new perspectives future

Language: Английский

Citations

6