Acute lung injury (ALI) is a major cause of morbidity and mortality globally, and is characterized by widespread inflammation in the lungs. Increased production of reactive oxygen species is hypothesized to be associated with ALI. Matrine and lycopene are active products present in traditional Chinese medicine. Matrine is an effective inhibitor of inflammation, whereas lycopene decreases lipid peroxidation. Therefore, it was hypothesized that combinatorial treatment with matrine and lycopene may provide synergistic protection against ALI. In the present study, mice were treated with dexamethasone (DEX; 5 mg/kg), matrine (25 mg/kg), lycopene (100 mg/kg), and matrine (25 mg/kg) + lycopene (100 mg/kg) for 7 days prior to injury induction using lipopolysaccharide (LPS; 5 mg/kg) for 6 h. Lung tissues were collected following the sacrifice of the mice and hematoxylin and eosin staining was used for histological analysis. Malondialdehyde (MDA), glutathione (GSH) and myeloperoxidas (MPO) levels were examined by respective kits. The expressions of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) were evaluated by ELISA. The expressions of IκBα and NF‑κB p65 were examined by reverse transcription‑quantitative polymerase chain reaction, western blotting and immunohistochemistry. The results indicated that the combined treatment exhibited a similar effect to DEX, both of which attenuated lung structural injuries, downregulated the expressions of IL‑6, TNF‑α, MPO and MDA, and upregulated that of GSH. Furthermore, the combined treatment and DEX inhibited NF‑κB p65 activation. The present study revealed that combined treatment with matrine and lycopene exhibited protective effects on an LPS‑induced mouse model of ALI, suggesting that they may serve as a potential alternative to glucocorticoid therapy for ALI.

Background: The basement membrane (BM), as a critical component of the extracellular matrix, plays a role in cancer progression. However, the role of the BM in lung adenocarcinoma (LUAD) remains unclear.

Spaceflight and microgravity environments have been shown to cause significant health impairments, including bone loss, immune dysfunction, and hematopoietic disorders. Hematopoietic stem cells (HSCs), as progenitors of the hematopoietic system, are critical for the continuous renewal and regulation of immune cells. Therefore, elucidating the regulatory mechanisms governing HSC fate and differentiation in microgravity environments is of paramount importance. In this study, hindlimb unloading (HU) was employed in mice to simulate microgravity conditions. After 28 days of HU, cells were isolated for analysis. Flow cytometry and colony-forming assays were utilized to assess changes in HSC proliferation and differentiation. Additionally, transcriptomic and untargeted metabolomic sequencing were performed to elucidate alterations in the metabolic pathways of the bone marrow microenvironment and their molecular regulatory effects on HSCs fate. Our findings revealed that 28 days of HU impaired hematopoietic function, leading to multi-organ damage and hematological disorders. The simulated microgravity environment significantly increased the HSCs population in the bone marrow, particularly within the long-term and short-term subtypes, while severely compromising the differentiation capacity of hematopoietic stem/progenitor cells. Transcriptomic analysis of HSCs, combined with metabolomic profiling of bone marrow supernatants, identified 1,631 differentially expressed genes and 58 metabolites with altered abundance. Gene set enrichment analysis indicated that HU suppressed key pathways, including hematopoietic cell lineage and MAPK signaling. Furthermore, integrated analyses revealed that metabolites affected by HU, particularly hypoxanthine enriched in the purine metabolism pathway, were closely associated with hematopoietic cell lineage and MAPK signaling pathways. Molecular docking simulations and in vitro experiments confirmed that hypoxanthine interacts directly with core molecules within these pathways, influencing their expression. These findings demonstrate that hypoxanthine in the bone marrow supernatant acts as a signaling mediator under microgravity, influencing HSCs fate by modulating hematopoietic cell lineage and MAPK signaling pathways. This study offers novel insights into the impact of microgravity on HSC fate and gene expression, underscoring the pivotal role of bone marrow microenvironmental metabolic changes in regulating key signaling pathways that determine hematopoietic destiny. Microgravity promotes the expansion of HSCs in the bone marrow by inhibiting cell cycle progression and reducing apoptosis. Microgravity suppresses the differentiation and function of HSPCs in the bone marrow. Microgravity alters purine metabolism in the bone marrow microenvironment, thereby affecting the MAPK signaling pathway and the hematopoietic cell lineage, ultimately regulating the fate of hematopoietic stem cells.

Respiratory diseases rank among the foremost causes of mortality and disability globally, with long-term exposure to environmental pollutants playing a critical role in their onset and progression. Despite this, the underlying mechanisms and effective targeted treatments for these disorders remain poorly understood, highlighting an urgent need for focused research. Cell death, a programmed cellular response to external harmful stimuli, including ferroptosis—a recently identified form of iron-dependent programmed cell death—emerges as a pivotal process. Characterized by intracellular iron accumulation and lipid peroxidation, ferroptosis appears intricately linked to lung injury induced by environmental pollutants. This review examines the role of ferroptosis in lung diseases triggered by environmental factors, aiming to shed light on its specific pathophysiological mechanisms and potential as a therapeutic target. By deepening our understanding of the interactions between environmental pollution, ferroptosis, and lung damage, we hope to inform strategies for effective intervention.