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Gene expression profiling of lung tissue from LPS-induced acute lung injury mice treated with Renshen Baidu Powder

ABSTRACT: This dataset presents transcriptomic profiles of lung tissue from a murine model of LPS-induced acute lung injury (ALI) following treatment with Renshen Baidu Powder (RSBD). LPS induced a robust inflammatory gene signature, which was significantly reversed by RSBD.

ORGANISM(S): Mus musculus

PROVIDER: GSE325662 | GEO | 2026/03/26

REPOSITORIES: GEO

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Tangeretin alleviates LPS-induced acute lung injury by inhibiting ferroptosis of macrophage via Nrf2 pathways

Project description:Sepsis-induced acute lung injury (ALI) is a severe clinical condition with a high mortality rate. Tangeretin, widely found in citrus fruits, has been reported to exert antioxidant and anti-inflammatory properties. However, whether Tangeretin protects against sepsis-induced ALI and the potential mechanisms remain unclear.We established ALI model via intraperitoneally injected with 5 mg/kg lipopolysaccharides (LPS) for 12 h. Tangeretin was applied intraperitoneally 30 min before LPS treatment. The lung tissue samples from both the LPS and LPS + TAN groups were subjected to RNA sequencing analysis, conducted by OE Biotech Co., Ltd. (Shanghai, China). We performed differential gene expression analysis using RNA-seq data between LPS and LPS/Tangeretin group.GSEA analysis between LPS and LPS/Tangeretin group showed that IL6_JAK_STAT3_SIGNALING, INFLAMMATORY_RESPONSE, TNFA_SIGNALING_VIA_NFKB were significantly enriched (Fig.3C-E). These results identified the anti-inflammatory effect of Tangeretin against sepsis-induced ALI.

2024-01-20 | GSE252755 | GEO

Time-resolved lung proteome profiling in an LPS-induced acute lung injury mouse model

Project description:This project investigates the dynamic lung proteome in a murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). C57BL/6N mice were exposed to LPS via intratracheal nebulization to induce ALI, and lung tissues were collected at multiple time points (non-stimulated controls, and days 1, 3, 7 and 14 after LPS challenge) to capture the onset, peak and resolution phases of lung injury.

2025-12-06 | PXD071688 |

Macrophage SH3GLB1 is required for Rab7-1 mediated mitophagy in inflammation during acute lung injury

Project description:Acute lung injury (ALI) accompanied by an inflammatory response is an important complication after drowning. Macrophage activation and polarization are implicated in the inflammatory process of lipopolysaccharide (LPS)-induced ALI (LPS-ALI), but little is known about drowning-induced ALI (drowning-ALI). SH3GLB1 is a member of the endophilin family and has been shown to be involved in mitochondrial morphological changes and autophagy. However, its role in ALI remains unclear. Here,we performed single-cell profiling of lung immune cells isolated from the lungs of drowning-ALI mouse models. We found that the regulation of macrophages in drowning-ALI was similar to that in LPS-ALI. Specifically, SH3GLB1 was highly expressed in macrophages of drowning-ALI mouse models and was related to inflammation. Furthermore, SH3GLB1 deletion ameliorated LPS-ALI or drowning-ALI. In contrast, the restoration of SH3GLB1 expression provoked LPS-ALI and drowning-ALI. Mechanistically, SH3GLB1 was shown to interact with Rab7 to contribute to mitophagy, which resulted in mitochondrial dysfunction. Overall, these findings indicated that SH3GLB1 is required for Rab7-mediated mitophagy in inflammation during ALI and could be a novel target for lung protection.

2026-02-10 | PXD073650 | Pride

Inhibition of GGPPS1 attenuated LPS-induced acute lung injury by suppressing the NLRP3 inflammasome

Project description:Rationale: Geranylgeranyl pyrophosphate synthase large subunit 1 (GGPPS1), a catalase downstream of the mevalonate pathway, regulates various pathological processes through balancing the production of farnesyl pyrophosphate and geranylgeranyl pyrophosphate. We sought to investigate whether GGPPS1 plays a role in mediating acute lung injury (ALI) using a mouse model of inflammation. Methods: Lipopolysaccharide (LPS) was intra-tracheally instilled to induce ALI in lung specific GGPPS1 knockout and wild-type mice. Expression of GGPPS1 in lung tissues and alveolar epithelial cells (AECs) was examined at different time points. Alveolar exudate, neutrophil infiltration, lung injury and cell death were determined. Change in global gene expression in response to GGPPS1 depletion was measured using mRNA microarray and verified in vivo and in vitro. Results: GGPPS1 levels increased significantly in lung tissues from LPS-induced ALI mice, where it showed a time- and dose-dependent increase in alveolar epithelial cells. Specific deletion of pulmonary GGPPS1 reduced the alveolar exudate and attenuated the severity of lung injury through inhibiting apoptosis of AECs. However, GGPPS1 deletion had limited effect on neutrophil counts and TNF-α levels in alveolar fluids. Deletion of GGPPS1 inhibited LPS-induced inflammasome activation, in terms of IL-1β release and pyroptosis, by down-regulating NLRP3 expression. Conclusions: Inhibition of pulmonary GGPPS1 attenuated LPS-induced ALI, predominantly by suppressing NLRP3 inflammasome activation.

2017-08-15 | GSE89311 | GEO

Comprisons of lung tissue gene expression from AKR and C57BL/6 mice exposed to Cigarette smoke and LPS in ARDS/ALI mice model

Project description:Our previous study showed that AKR and C57BL/6 mice to cigarette smoke increased lipopolysaccharide (LPS)- induced increased lung vascular permeability. Viremic AKR mice were more susceptible to LPS-induced ALI than C57 on prolonged exposure. In this study we compared the global gene expression patterns to determine the genetic basis for the strain dependent responses to cigarette smoke and LPS-induced ALI. We found AKR transcriptomic responses didnot overlap with C57 mice and AKR mice showed increased responses compared to C57 mice. Global gene expression analysis using microarray was used to dermine the mechanisms of strain dependent responses to cigarette smoking and LPS mediated ALI

2023-05-28 | GSE193958 | GEO

Multi-omics Analysis Reveals the Effects of LPS-induced Acute Lung Injury in Mice

Project description:To investigate the molecular alterations in the pathogenesis of ALI induced by LPS. We then performed gene expression profiling analysis using data obtained from RNA-seq of lung tissues from the two comparison groups.

2023-11-11 | GSE216943 | GEO

Gene expression profiling of lung tissue from LPS-induced acute lung injury mice treated with Renshen Baidu Powder

Project description:Gene expression profiling of lung tissue from LPS-induced acute lung injury mice treated with Renshen Baidu Powder

| PRJNA1441433 | ENA

Synergistic Therapeutic Effects of D-Mannitol-Cerium-Quercetin (Rutin) Coordination Polymer Nanoparticles on Acute Lung Injury

Project description:In our latest study, we pioneered the use of D-Mannitol-Cerium-Quercetin/Rutin coordination polymer nanoparticles (MCQ/R NPs) as a potential remedy for ALI. our in vivo studies with LPS-induced ALI mice showed significant mitigation of lung tissue inflammation. This groundbreaking research presents MCQ/R NPs as a prospective vanguard in ALI therapeutics by proteomics.

2024-04-10 | PXD051350 |

Andrographolide sulfonate attenuates acute lung injury by reducing expression of myeloperoxidase and neutrophil-derived proteases in mice

Project description:Andrographolide sulfonate (Andro-S), a sulfonation derivative of andrographolide, is known to be effective in treating inflammation-related diseases, while the underlying mechanisms and global protein alterations in response to Andro-S remain unknown. This study aimed to investigate the pharmacological effects and potential targets of Andro-S in a murine model of acute lung injury (ALI). ALI was induced by aerosolized lipopolysaccharide (LPS) exposure before treatment with Andro-S. Inflammatory state of each treatment group was determined by histological analysis and quantification of inflammatory markers. Differentially expressed proteins in lung tissues were identified by an iTRAQ-based quantitative proteomic approach and further confirmed by immunohistochemistry analysis. Administration of Andro-S alleviated LPS-induced histological changes in the lung and reduced the expression of inflammatory markers in serum, bronchoalveolar fluid and lung tissues. Proteomic analysis identified 34 differentially expressed proteins from a total of 2,234 quantified proteins in the lung. According to bioinformatics analysis, neutrophil elastase (ELANE), Cathepsin G (CTSG) and myeloperoxidase (MPO), three neutrophil-derived proteases related to immune system process and defense responses to fungi were chosen as potential targets of Andro-S. Further immunohistochemistry analysis confirmed the inhibitory effects of Andro-S on LPS-induced ELANE, CTSG and MPO up-regulation. These results indicate that Andro-S suppressed the severity of LPS-induced ALI, possibly by attenuating the expression of and neutrophil-derived proteases.

2018-10-22 | PXD008552 | Pride

Nogo-B protects mice against lipopolysaccharide-induced acute lung injury

Project description:Purpose: Acute lung injury (ALI) is a severe clinical disorder characterized by diffused capillary-alveolar barrier damage and noncardiogenic lung edema induced by excessive inflammation reactions. Nogo-B, a member of the reticulon 4 protein family, plays a critical role in modulating macrophages and neutrophils’ function in inflammation. Its role in ALI remains unclear. Methods: Pulmonary expression of Nogo-B was investigated in a LPS-induced ALI mice model. The effects and the underline mechanisms of Nogo-B expression on the severity of lung injury was assessed using histological examination, Bronchoalveolar lavage fluid (BALF) protein and inflammatory cells and cytokines measurement, and microarray analysis. Results: Nogo-B was normally highly expressed in the lungs of naïve C57BL/6 mice. Intra-tracheal instillation of LPS significantly repressed the Nogo-B expression in lung tissues and BALF cells of ALI mice. In addition, over-expression of pulmonary Nogo-B using an adenovirus vector which expresses a Nogo-B-RFP-3-flag fusion protein (Ad-Nogo-B) significantly prolonged the survival time of mice challenged with lethal dose of LPS. Histological results and BALF protein measurement convinced that Ad-Nogo-B treated mice had less severity of lung injury and alveolar protein exudation, as compared with control adenovirus treated mice (Ad-RFP). They also had higher MCP-1 secretion and alveolar macrophages infiltration, but lower neutrophils infiltration. Finally, using microarray analysis, we identified a protective gene, PTX3, was highly elevated in Ad-Nogo-B treated mice. Conclusions: Nogo-B played a protective role in LPS-induced ALI, which might exert its role through modulation of inflammatory response and PTX3 secretion. A total of 12 samples from mice treated with or without LPS in the presence of Ad-Nogo-B or Ad-RFP transfection (n=3 for each group)

2013-07-12 | E-GEOD-48787 | biostudies-arrayexpress

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