Search Results (949)

Background/Objectives: Growth differentiation factor-15 (GDF-15) is a protein that belongs to the transforming growth factor beta superfamily and has been found elevated in cases of organ injury such as liver, kidney, heart, and lung, as well as cardiovascular diseases and cancer. Soluble urokinase plasminogen activator receptor (suPAR) is a protein which is expressed mainly on immune cells and endothelial and smooth muscle cells, and is a marker of severity and intensity of inflammation in acute and chronic diseases. The aim of the present study was to compare GDF-15 serum levels between patients with acute cerebrovascular incidents and healthy controls and to investigate the possible correlation of GDF-15 serum levels and inflammatory markers, such as serum C-reactive protein (CRP) and plasma suPAR, in the above-mentioned groups. Methods: This is a retrospective study. Thirty-one patients were included in the study, with a mean age ± SD of 67 ± 13 years, compared to 18 age-matched healthy controls. Results: In the patient group a statistically significant positive correlation of serum levels of GDF15 values with suPAR and CRP emerged (rs = 0.516, p = 0.003) and (rs = 0.409, p = 0.022), respectively, and no significant correlation was found in the group of controls (rs = 0.271, p = 0.277) and (rs = 0.423, p = 0.080), respectively. Conclusions: These findings support the role of inflammation as a key underlying mechanism in acute cerebrovascular injury and suggest that GDF-15 may serve as a valuable adjunct biomarker for assessing disease severity and inflammatory burden. Full article

Inhibiting epithelial sodium channel (ENaC) provides clinical benefit in cystic fibrosis treatment, whereas activated alveolar ENaC attenuates acute lung injury/acute respiratory distress syndrome. However, seldom bibliometric analysis of respiratory ENaC systematically evaluates hotspots and trends in ion transport, as well as providing few overviews for researchers. This review aims to provide a comprehensive overview of respiratory ENaC over the past 40 years, identifying the research frontier and topic evolution. Searching the literature in Science Citation Index Expanded from Web of Science (WOS) and PubMed, a total of 1634 publications in 409 journals, authored by 5457 researchers from 60 countries/regions, were analyzed by CiteSpace, VOSviewer, and sciMAT software. The earliest highly cited article, titled ‘Rescue of CF airway epithelial cell function in vitro by a CFTR potentiator, VX-770’, had accumulated 1011 citations. The most prolific author, country, and journal were MA Mall, USA, and Am J Physiol Lung Cell Mol Physiol, respectively. In the most recent phase of annual focus, research areas could be clustered by immunology, cell biology, pharmacology and pharmacy, biotechnology and applied microbiology, and physiology. In summary, this bibliometric research reveals that respiratory ENaC is not only responsible for alveolar fluid clearance, but has converted into a broader modulator in immune-inflammatory responses. Full article

Background: Magnetic particle imaging (MPI) is an emerging, tracer-based modality that directly detects superparamagnetic iron oxide nanoparticles (SPIONs) with exceptional sensitivity, quantitative signal behavior, and full immunity to air–tissue susceptibility artifacts. These features make MPI particularly well-suited for pulmonary imaging, where traditional techniques such as computed tomography (CT), magnetic resonance imaging (MRI), and nuclear medicine-based ventilation/perfusion (V/Q) imaging are limited by radiation exposure, low contrast, and motion-related signal degradation. Objective: This review synthesizes the current state of MPI for lung imaging, with emphasis on its physical principles, tracer development, preclinical applications, and its potential role in assessing pulmonary perfusion, vascular integrity, inflammation, and therapeutic responses. Methods: A systematic evaluation of preclinical studies was performed across three major application domains: pulmonary perfusion mapping, cell tracking and therapeutic monitoring, and vascular injury and permeability assessment. Study designs, SPION formulations, MPI acquisition strategies, and validation methods, including histopathology, biodistribution, broncho-alveolar lavage fluid (BALF) analysis, and Evans Blue assays, were examined to characterize methodological consistency and imaging performance. Results: MPI consistently demonstrated high-contrast, quantitative visualization of pulmonary blood flow, endothelial barrier disruption, inflammatory signaling, and transplanted or inhaled cell populations. Tracer engineering played a critical role: macroaggregated albumin superparamagnetic iron oxide nanoparticles (MAA-SPIONs) enabled capillary-level perfusion mapping, LS-008 improved temporal resolution and vascular delineation, Synomag/Synomag-D allowed quantification of vascular leakage in acute and chronic lung injury, and vascular cell adhesion molecule-1 (VCAM-1)-targeted probes provided molecular-level assessment of inflammation. Hybrid MPI-CT and MPI-MRI approaches further enhanced anatomic localization and enabled accurate pulmonary blood volume (PBV) estimation. Across studies, MPI measurements showed strong agreement with established biological assays and remained free of the artifacts that limit CT and MRI in the lung. Conclusions: Preclinical evidence demonstrates that MPI is a robust, radiation-free, and quantitatively precise modality for functional and molecular lung imaging. Its ability to map perfusion, track therapeutic agents, and noninvasively quantify vascular permeability positions MPI as a promising future alternative or complement to CT, MRI, and nuclear medicine for pulmonary assessment. Continued tracer optimization, system scaling, and clinical validation are key steps toward translating MPI into routine clinical use. Full article

Background/Objectives: Sepsis is a life-threatening syndrome arising from a dysregulated host response to infection, frequently leading to multiple organ dysfunction, with the lungs being among the most severely affected organs. Oxidative stress, inflammation, apoptosis, and DNA damage play key roles in the pathogenesis of sepsis-induced acute lung injury (ALI). Beyond its lipid-lowering effects, rosuvastatin possesses anti-inflammatory and antioxidant properties that may confer protective effects in sepsis. This study was designed to investigate the dose-dependent prophylactic efficacy of rosuvastatin in mitigating pulmonary damage in rats with cecal ligation and puncture (CLP)-induced sepsis. Methods: Sprague–Dawley rats were randomly divided into six groups: Sham, Sham + rosuvastatin (10 mg/kg), Sham + rosuvastatin (20 mg/kg), CLP, CLP + rosuvastatin (10 mg/kg), and CLP + rosuvastatin (20 mg/kg). Rosuvastatin was administered via oral gavage 4 h before the surgical procedures in the experimental groups. All animals were sacrificed 16 h following surgical procedures. Lung tissues were analyzed for biochemical markers, including malondialdehyde (MDA) and reduced glutathione (GSH), as well as histopathological changes and immunohistochemical expression of NF-κB/p65, caspase-3, and 8-OHdG. Results: CLP-induced sepsis significantly increased MDA levels while decreasing GSH levels, indicating enhanced oxidative stress. Rosuvastatin treatment significantly reversed these changes. Histopathological analysis revealed marked lung injury in the CLP group, including alveolar inflammation, interstitial inflammation, vascular congestion, and increased alveolar septal thickness, all of which were significantly reduced following rosuvastatin administration. Immunohistochemical findings demonstrated increased expression of NF-κB/p65, caspase-3, and 8-OHdG in the CLP group, whereas rosuvastatin significantly attenuated these expressions. No significant difference in prophylactic efficacy was observed between the 10 mg/kg and 20 mg/kg doses of rosuvastatin. Conclusions: Rosuvastatin demonstrated a protective effect against sepsis-induced pulmonary damage by reducing oxidative stress, inflammation, apoptosis, and DNA damage. These findings suggest that rosuvastatin may have prophylactic potential in sepsis; however, further support is needed from investigations of cellular pathways in different mechanistic directions. Full article

Acute respiratory distress syndrome (ARDS) is characterized by systemic inflammation, immune dysregulation, oxidative stress, and frequent extrapulmonary organ involvement. Neurological complications of ARDS, such as neuroinflammation, cognitive impairment and delirium, are common and worsen outcomes. Early evidence highlights bidirectional communication between the lungs and brain, the lung–brain axis, through which inflammation may amplify both pulmonary and cerebral injury. This narrative review synthesizes recent experimental and clinical data on the immunomodulatory and neuroprotective effects of commonly used sedative agents in ARDS, focusing on their influence on inflammatory mediators (IL-1β, IL-6, IL-8, IL-10, TNF-α) and neuronal injury biomarkers (S100B, neuron-specific enolase). Sedative agents seem to exert effects beyond sedation by modulating systemic and neuroinflammatory responses. Evidence suggests they can influence cytokine profiles and reduce biomarkers associated with neuronal injury, potentially mitigating neuroinflammation and delirium in ARDS patients. Sedatives may modulate lung–brain crosstalk in ARDS through immunoinflammatory pathways, integrating sedative and neuroprotective effects. Mechanistic clarification may enable targeted sedation strategies to improve pulmonary and neurological outcomes. Full article

Endotoxemia represents a life-threatening clinical disorder driven by an aberrant host immune response to pathogenic infection, often resulting in severe multiple organ dysfunction. Among its most devastating complications are acute lung injury (ALI) and endotoxemia-associated encephalopathy (EAE), both of which are associated with elevated mortality and currently lack effective targeted interventions. This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia. Our results showed that treatment with rhTβ4 markedly enhanced survival rates and diminished the systemic overproduction of diverse proinflammatory cytokines and chemokines in endotoxemic mice. These systemic protective actions were achieved through the inhibition of the TLR4/NF-κB signaling cascade, the reduction in M1 macrophage polarization, and the simultaneous alleviation of mitochondrial impairment and oxidative stress. Moreover, rhTβ4 treatment significantly rescued EAE-related cognitive deficits and attenuated neuronal damage, primarily through the suppression of neuroinflammation and microglial overactivation. Integrative transcriptomic profiling and functional assays identified lysophosphatidic acid receptor 3 (LPAR3) as an important contributor, suggesting that rhTβ4 suppresses microglial-mediated neurotoxicity at least in part through LPAR3 downregulation. In conclusion, rhTβ4 confers robust multi-organ protection against endotoxemic injury by orchestrating the inhibition of systemic and central neuroinflammatory cascades, positioning it as a promising candidate for the treatment of endotoxemia-induced ALI and EAE. Full article

Radiotherapy remains one of the main pillars of cancer treatment and is used in more than half of all oncological patients. Despite continuous technological improvements, ionizing radiation inevitably causes damage to surrounding healthy tissues, leading to acute and chronic complications affecting multiple organs, including the skin, mucosa, heart, lungs, bones and gastrointestinal tract. Radiation-induced injuries significantly impair patients’ quality of life, limit therapeutic doses, and represent a major unmet clinical challenge. Hydrogels have emerged as promising biomaterials for managing radiation-induced damage due to their high content of water, tunable mechanics, and ability to mimic the extracellular matrix. Recent innovations have introduced functional systems, including stimuli-responsive, injectable, and bioactive hydrogels, capable of delivering antioxidants, growth factors, or living cells. Unlike traditional material-based reviews, this work proposes a novel classification framework based on the hydrogel’s mechanism of action within the pathophysiology of radiation injury. We evaluate how specific designs, such as ROS-scavenging matrices, barrier-forming injectable shields, and bioactive delivery vehicles, address distinct phases of inflammation and fibrosis. By providing a comprehensive overview of radiation-induced injuries across different organs, this review summarizes current hydrogel-based strategies for both prevention and therapy. We highlight the potential of these mechanistically aligned systems to protect healthy tissues, suppress chronic inflammation, and promote effective tissue regeneration. Full article

Background: Aspirin, initially recognized for its anti-inflammatory, antipyretic and analgesic properties, holds a prominent role in the treatment of cardiovascular disease. The utility of aspirin in cancer therapeutics has been explored and stratified into COX-dependent and -independent mechanisms. COX2 gene expression has been demonstrated to be significantly upregulated in colorectal cancer and various other gastrointestinal malignancies including pancreatic, esophageal, and gastric cancer. This study investigates the relationship of aspirin use and outcomes in patients with colorectal cancer. Methods: The Nationwide Inpatient Sample (NIS) database from 2017 to 2022 was analyzed for patients age > 18 who were hospitalized for colorectal cancer and its decompensations using ICD-10 diagnostic codes. These patients were further stratified based on the long-term use of aspirin. The principal outcome of this investigation are the odds of in-hospital mortality, with secondary outcomes including odds of pulmonary embolism, portal vein thrombosis, acute kidney injury, septic shock, requiring an ICU level of care and odds of hepatic, pulmonary, gastrointestinal and peritoneal or retroperitoneal metastatic disease. Multivariate logistic regression accounting for hospital and patient characteristics was implemented for analysis, with the Charlson Comorbidity Index used to adjust for coexisting comorbidity burden; a p-value (p) of <0.05 was considered statistically significant. Results: In our analysis of the NIS, 596,160 patients were identified with colorectal cancer and 11.7% (69,750) of this population were identified with long-term use of aspirin. Aspirin use was identified to have a significantly reduced odds of in-patient mortality (adjusted odds ratio) [aOR] 0.530, p value < 0.001 95% CI (confidence interval): 0.460–0.617. Patients with aspirin use also demonstrated significantly reduced odds of adverse outcomes and gastrointestinal, hepatic, pulmonary and retroperitoneal/peritoneal metastasis; (aOR 0.606, 95% CI: 0.564–0.653, p < 0.001), (aOR 0.628, 95% CI: 0.582–0.678, p < 0.001), (aOR 0.676, 95% CI: 0.605–0.755, p < 0.001) and (aOR 0.751, 95% CI: 0.685–0.825, p < 0.001) respectively. Conclusions: In recent years, there has been an alarming increase in incidence of colorectal cancer, particularly amongst younger individuals with increased associated mortality. This mortality increase, albeit alarming, is a driving force for treatment innovation with continual examination of our repertoire of medications for possible repurposed applications. COX2-mediated signaling serves as a key promotor of tumorigenic molecular signaling that directly contributes to tumor cell proliferation, angiogenesis and metastasis in colorectal cancer. Aspirin use and its inhibitory action on COX2 demonstrated a significantly reduced odds of in-hospital mortality. Aspirin use is also associated with significantly reduced odds of developing metastatic disease to the liver, gastrointestinal system, lungs and peritoneum in patients with colorectal cancer. These findings convey that aspirin use reduces the likelihood of in-hospital mortality, major comorbid conditions and of developing metastatic disease as compared to those who do not use aspirin. Full article

Background: Acute lung injury (ALI) is a major contributor to mortality in neonatal sepsis, yet the mechanisms underlying early lung damage remain incompletely understood. Although extracellular traps (ETs) have been implicated in inflammatory injury, the cellular origin and regulatory pathways of ET formation in neonatal sepsis remain unclear. This study aimed to determine the source of ETs and to investigate the role of hypoxia-inducible factor-1α (HIF-1α) in regulating macrophage extracellular traps (METs) formation and lung injury. Methods: Neonatal sepsis was induced in mice by intraperitoneal injection of cecal slurry. METs formation was assessed by immunofluorescence staining, Western blotting, and extracellular DNA quantification. Selective depletion of macrophages or neutrophils was performed to determine the cellular source of ETs. In vitro experiments were conducted using macrophages stimulated with lipopolysaccharide or phorbol 12-myristate 13-acetate. RNA sequencing analysis and pharmacological inhibition were used to examine the roles of HIF-1α, glycolysis, and enolase 2 (ENO2) in METs formation, lung injury, and survival outcomes. Results: We identify macrophages as a predominant source of ETs in the lung and demonstrate that METs contribute to lung injury in neonatal sepsis. Depletion of macrophages or pharmacological inhibition of METs formation markedly attenuated lung injury and improved survival in neonatal sepsis mice. Mechanistically, we suggest that HIF-1α promotes METs formation by driving glycolysis in macrophages. Furthermore, this process appears to involve the upregulation of key glycolytic enzymes, including ENO2, potentially facilitating METs release. In turn, METs are implicated in enhancing macrophage inflammatory activation, which could exacerbate lung injury. Importantly, pharmacological targeting of HIF-1α pathways reduces METs formation, attenuates lung inflammation, and improves survival outcomes. Conclusions: These findings suggest a role for HIF-1α in regulating METs formation and support that targeting this pathway could represent a potential therapeutic strategy for neonatal sepsis-associated acute lung injury. Full article

Background/Objectives: Immune checkpoint inhibitors (ICIs) have transformed cancer therapy, providing substantial survival benefits across a wide range of malignancies. However, ICI-associated renal toxicity encompasses a broad spectrum of clinical entities, ranging from nonspecific acute kidney injury to well-defined immune-mediated nephropathies with distinct pathophysiological mechanisms. Methods: We performed a large-scale pharmacovigilance study using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) database to evaluate immune-mediated nephropathy associated with ICIs from January 2014 to March 2025. To improve specificity and minimize misclassification, the analysis was restricted to well-defined immune-mediated renal adverse events identified using MedDRA Preferred Terms, excluding nonspecific acute kidney injury. Disproportionality analysis was conducted using reporting odds ratios (RORs) with 95% confidence intervals (CIs) to assess associations between individual ICIs, treatment regimens, and nephropathy reporting. Results: Among 203,652 ICI-related adverse event reports (irAEs), 2361 (1.12%) involved immune-mediated nephropathy. Compared with other irAEs (non-nephropathy), immune-mediated nephropathy was more frequently reported in patients aged ≥ 65 years and in those with lung and genitourinary malignancies. Tubulointerstitial nephritis was the predominant subtype. Higher reporting signals were observed with cemiplimab and pembrolizumab, whereas durvalumab and atezolizumab demonstrated lower reporting signals. Combination regimens involving PD-1 and CTLA-4 inhibitors were associated with higher reporting frequencies compared with monotherapy. Conclusions: This real-world pharmacovigilance analysis identifies clinically relevant differences in immune-mediated nephropathy reporting across ICI classes and treatment strategies. PD-1 inhibitors and PD-1/CTLA-4 combination regimens were associated with higher reporting signals, suggesting potential variation in renal safety profiles. These findings should be interpreted cautiously, given the inherent limitations of spontaneous reporting systems, but they provide hypothesis-generating evidence to support future prospective studies with detailed clinical and histopathological correlation. Full article

Inflammatory lung diseases are characterized by complex immune dysregulation and structural tissue damage, demanding the development of novel therapeutic and diagnostic strategies. Exosomes (Exos) have emerged as promising alternatives to address these challenges by serving as key mediators and effective therapeutic nanocarriers. This review systematically analyzes the multifunctional roles of Exos derived from various sources, including immune cells, mesenchymal stem cells (MSCs), lung structural cells, and non-mammalian sources such as plants and milk, in the context of inflammatory lung diseases. These vesicles modulate critical pathological processes, such as macrophage polarization, oxidative stress, and programmed cell death, by delivering functional cargos, including miRNAs and proteins. Studies demonstrating the antioxidant properties of Exos are classified, and their roles in attenuating oxidative stress-mediated lung injury are discussed. Furthermore, engineering and priming strategies, as well as airway-directed delivery methods such as nebulization, are reported to enhance therapeutic efficacy and targeting. Evidence also indicates that plant-derived Exos could be scalable and safer alternatives to mammalian cell-derived Exos. Collectively, Exos represent a next-generation platform for precision medicine, functioning as potent therapeutic agents and efficient drug-delivery systems for the treatment of complex inflammatory lung diseases. Full article

WNT5a is a lipid-modified glycoprotein member of the WNT family of signaling molecules. Two isoforms of WNT5a have been identified that are conserved across mice and humans. These isoforms display specific functions in regulating cancer cell activities. While WNT5a is, indeed, essential for normal lung development and homeostasis, and is dysregulated in multiple lung diseases, little to no information is available regarding the expression or potential function of WNT5a isoforms in normal or diseased lungs. Such information has the potential to help to elucidate the more precise and nuanced functions of WNT5a in various pulmonary conditions. In this study, we characterized the expression of individual Wnt5a isoforms during mouse lung development and compared their expression across major alveolar cell populations. We further investigated the molecular basis of the signaling mechanisms that regulate Wnt5a isoform expression in fibroblasts, the major lung cell type with high-level Wnt5a expression. We present data that reveal a role for the AKT pathway in differentially regulating the expression of Wnt5a isoforms, a novel finding. Furthermore, we demonstrate that Wnt5a isoforms are dysregulated in bleomycin-induced fibrosis and Pseudomonas aeruginosa (PA)-induced acute lung injury and exhibit distinct impacts in Wnt5a isoform expression in response to lung injury. Full article

The dipeptidyl peptidase (DPP) family comprises enzymes with important metabolic and immunomodulatory properties. This narrative review summarizes recent clinical and experimental evidence on the role of DPP-1, DPP-4, DPP-9, and DPP-10 in pulmonary diseases. The strongest translational evidence currently supports DPP-1 inhibition in non-cystic fibrosis bronchiectasis, where brensocatib reduces exacerbations and prolongs time to first exacerbation, with additional DPP-1 inhibitors in development. By contrast, the roles of DPP-4, DPP-9, and DPP-10 are supported mainly by preclinical studies in pulmonary hypertension, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), pulmonary fibrosis, asthma, non-small cell lung cancer (NSCLC), and nonsteroidal anti-inflammatory drugs (NSAIDs)/aspirin-exacerbated respiratory disease. Across these models, DPP inhibition modulates inflammation, protease activation, epithelial- or endothelial-to- mesenchymal transition (EMT/ EndMT), extracellular matrix (ECM) remodeling, and related signaling pathways. Overall, DPP-targeted interventions are promising in pulmonary medicine, but broader clinical translation will require well-designed prospective trials. Full article

Background/Objectives: Methicillin-resistant Staphylococcus aureus (MRSA) is a multidrug-resistant pathogen that poses a major public health concern. It predominantly infects immunocompromised individuals and is frequently associated with severe pulmonary complications, including acute lung injury. Diosmetin, a natural flavonoid, known for its anti-inflammatory, antioxidant, and anti-infective properties. Nevertheless, its therapeutic mechanism in the treatment of acute pneumonia induced by MRSA remains unclear. Methods: In this study, we employed network pharmacology and molecular docking to elucidate the mechanisms underlying the therapeutic effect of diosmetin against MRSA-induced pneumonia. An MRSA pneumonia model was established in Balb/c mice. The impacts of diosmetin on murine pneumonia were evaluated by detecting biochemical indicators via HE staining, ELISA, RT-qPCR, and WB. In vitro experiments utilized RAW264.7 macrophages to establish an MRSA infection model for further validation of the therapeutic mechanisms of diosmetin. Results: In vivo results demonstrated that diosmetin alleviated MRSA-induced lung injury and reduced mortality by inhibiting the release of pro-inflammatory cytokines. Furthermore, compared with model mice, diosmetin-treated mice showed reduced phosphorylation levels of NLRP3, pro-caspase-1, ASC, and NF-κB p65, along with an increased level of IκBα in lung tissue. In vitro experiments indicated that diosmetin effectively reduced the levels of pro-inflammatory cytokines in MRSA-infected RAW264.7 macrophages and exerted anti-inflammatory effects by modulating the expression of NLRP3, pro-caspase-1, ASC, IκBα, and NF-κB p65. Conclusions: Our results demonstrate that diosmetin alleviates MRSA-induced pneumonia in mice, and this protective effect is achieved through dual inhibition of the NF-κB/NLRP3 inflammasome axis. Full article

Background: Acute lung injury (ALI) is a major complication of sepsis, driven by oxidative stress, inflammation, and apoptosis. Paeoniflorin, a monoterpenoid glycoside, has demonstrated notable antioxidant and anti-inflammatory properties, suggesting potential therapeutic value in ALI. Methods: Sepsis-induced ALI was established in mice using the cecal ligation and puncture (CLP) model. The protective effects of paeoniflorin were evaluated by measuring oxidative stress markers (SOD, GSH, and MDA) and pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) using biochemical assays and RT-PCR. Histopathological examination and apoptosis assessment (Bax and Bcl-2 expression) were performed. Western blot analysis was conducted to investigate the involvement of the JAK2/STAT3 signaling pathway. Network pharmacology analysis was used to identify potential molecular targets, and molecular docking was performed to explore binding interactions. Results: CLP-induced ALI resulted in increased oxidative stress and inflammatory responses, as evidenced by elevated MDA and cytokine levels, along with reduced SOD and GSH levels. Paeoniflorin treatment significantly ameliorated these alterations. Histological damage and apoptosis were markedly reduced, accompanied by the downregulation of Bax and upregulation of Bcl-2. Additionally, paeoniflorin inhibited activation of the JAK2/STAT3 pathway. Network pharmacology identified key ALI-related targets, including IL6, TNF, IL1B, HIF1A, STAT3, NFKB1, CCL2, CYBB, CXCL8, and NOX4. Molecular docking revealed strong binding affinity of paeoniflorin toward HIF-1 and JUN, and moderate interactions with IL-1β, TNF-α, and Bax. Conclusions: Paeoniflorin exerts protective effects against sepsis-induced ALI by attenuating oxidative stress, inflammation, and apoptosis, partly through inhibition of the JAK2/STAT3 signaling pathway. These findings highlight its potential as a promising therapeutic candidate for ALI management. Full article