Sex hormones in COVID-19 severity: The quest for evidence and influence mechanisms.

Studies have reported variable effects of sex hormones on serious diseases. Severe disease and mortality rates in COVID-19 show marked gender differences that may be related to sex hormones. Sex hormones regulate the expression of the viral receptors ACE2 and TMPRSS2, which affect the extent of viral infection and consequently cause variable outcomes. In addition, sex hormones have complex regulatory mechanisms that affect the immune response to viruses. These hormones also affect metabolism, leading to visceral obesity and severe disease can result from complications such as thrombosis. This review presents the latest researches on the regulatory functions of hormones in viral receptors, immune responses, complications as well as their role in COVID-19 progression. It also discusses the therapeutic possibilities of these hormones by reviewing the recent findings of clinical and assay studies.

Tyrosine kinase receptor B attenuates liver fibrosis by inhibiting TGF-ß/SMAD signaling.

BACKGROUND AND AIMS: Liver fibrosis is a leading indicator for increased mortality and long-term comorbidity in NASH. Activation of HSCs and excessive extracellular matrix production are the hallmarks of liver fibrogenesis. Tyrosine kinase receptor (TrkB) is a multifunctional receptor that participates in neurodegenerative disorders. However, paucity of literature is available about TrkB function in liver fibrosis. Herein, the regulatory network and therapeutic potential of TrkB were explored in the progression of hepatic fibrosis. METHODS AND RESULTS: The protein level of TrkB was decreased in mouse models of CDAHFD feeding or carbon tetrachloride-induced hepatic fibrosis. TrkB suppressed TGF-ß-stimulated proliferation and activation of HSCs in 3-dimensional liver spheroids and significantly repressed TGF-ß/SMAD signaling pathway either in HSCs or in hepatocytes. The cytokine, TGF-ß, boosted Nedd4 family interacting protein-1 (Ndfip1) expression, promoting the ubiquitination and degradation of TrkB through E3 ligase Nedd4-2. Moreover, carbon tetrachloride intoxication-induced hepatic fibrosis in mouse models was reduced by adeno-associated virus vector serotype 6 (AAV6)-mediated TrkB overexpression in HSCs. In addition, in murine models of CDAHFD feeding and Gubra-Amylin NASH (GAN), fibrogenesis was reduced by adeno-associated virus vector serotype 8 (AAV8)-mediated TrkB overexpression in hepatocytes. CONCLUSION: TGF-ß stimulated TrkB degradation through E3 ligase Nedd4-2 in HSCs. TrkB overexpression inhibited the activation of TGF-ß/SMAD signaling and alleviated the hepatic fibrosis both in vitro and in vivo . These findings demonstrate that TrkB could be a significant suppressor of hepatic fibrosis and confer a potential therapeutic target in hepatic fibrosis.

A H2O2-free heterogeneous Fenton process for the degradation of lincomycin using natural structural iron-containing clay mineral and dimethoxyhydroquinone with in situ generated hydroxyl radicals.

The heterogeneous Fenton process is a strategy for overcoming the greatest shortcomings of traditional homogeneous Fenton, i.e. the high generation of ferric hydroxide sludge and effectivity in a limited pH range. In this study, we constructed a heterogeneous Fenton system with natural iron-bearing clay mineral (nontronite) and dimethoxyhydroquinone (DMHQ) to degrade lincomycin (LCM) without the addition of H2O2. The degradation mechanism was derived from the hydroxyl radicals (•OH) produced from the oxygenation of Fe(II) in nontronites, which was reduced by DMHQ. Acidic conditions and low concentrations of LCM were favourable for LCM degradation. When the solution pH increased from 3 to 7, the final LCM removal ratio decreased from 95 to 46%. However, LCM can still be degraded by 46% under neutral conditions and 20% at the LCM concentration of 500 µmol/L. The nontronite has good reusability, and the LCM degradation efficiency in the fourth cycle still exceeded 90% of the original efficiency. The degradation sites of LCM mainly occurred in the methyl thioether moiety and the aliphatic amine group on the pyrrolidine ring, with the final product of CO2. This research presents a new eco-friendly and cost-effective method for the heterogenous Fenton process without external H2O2.

E-cadherin to N-cadherin switching in the TGF-ß1 mediated retinal pigment epithelial to mesenchymal transition.

A serious form of ocular fibrotic disease is proliferative vitreoretinopathy (PVR) that can ultimately lead to blindness. While the pathogenesis of PVR is known to be closely tied to retinal pigment epithelial (RPE) cell epithelial-mesenchymal transition (EMT) characterized by E-cadherin downregulation and N-cadherin upregulation. Herein, we developed a model of transforming growth factor-ß1 (TGF-ß1)-induced EMT using human RPE (hRPE) cells as a tool for exploring the mechanistic basis for E-cadherin to N-cadherin switching. This analysis revealed that the loss of E-cadherin led to the separation of ß-catenin from the catenin-cadherin complex whereupon it underwent nuclear entry to activate zinc finger E-box binding homeobox 1 (ZEB1), in turn promoting N-cadherin upregulation in this biological context. E-cadherin overexpression was sufficient to inhibit this EMT process and proliferation in RPE cells, further constraining their TGF-ß1-induced apoptosis.

Bifunctional Phenol-Enabled Sequential Polymerization Strategy for Printable Tough Hydrogels.

Hydrogels are promising material candidates in engineering soft robotics, mechanical sensors, biomimetic regenerative medicine, etc. However, developing multinetwork hydrogels with high mechanical properties and excellent printability are still challenging. Here, a bifunctional phenol-enabled sequential polymerization (BPSP) strategy is reported to fabricate high-performance multinetwork hydrogels under the orthogonal catalysis of efficient ruthenium photochemistry. Benefiting from this bifunctional design, phenols can sequentially polymerize with typical monomers and themselves to fabricate various phenol-containing polymers (Ph-Ps) and Ph-Ps-based multinetwork tough hydrogels, respectively. The as-prepared hydrogels have maximum stress of 0.75 MPa and toughness of 2.2 MJ m- 3 under the critical strain of 800%. These property parameters are a maximum of 16 times higher than those of the phenol-postmodified and phenol-free hydrogels. Moreover, the rapid coupling polymerization of phenols can shorten the gelation times of hydrogels to as low as ≈4 s, which enables its printable property for customizable applications. As a proof of concept, a 3D scaffold-like structure is optimized as highly sensitive mechanical sensors for detecting various human motions.

TSPAN4-positive migrasome derived from retinal pigmented epithelium cells contributes to the development of proliferative vitreoretinopathy.

BACKGROUND: Proliferative vitreoretinopathy (PVR) is a blind-causing disease initiated by the activation of retinal pigmented epithelium (RPE) primarily induced by TGF-ß families. Migrasome is a recently discovered type of extracellular vesicle related to cell migration. RESULTS: Here, we used ex vivo, in vitro, and in vivo models, to investigate the characteristics and functions of migrasomes in RPE activation and PVR development. Results indicated that the migrasome marker tetraspanin-4 (TSPAN4) was abundantly expressed in human PVR-associated clinical samples. The ex vivo model PVR microenvironment is simulated by incubating brown Norway rat RPE eyecups with TGF-ß1. Electron microscope images showed the formation of migrasome-like vesicles during the activation of RPE. Further studies indicated TGF-ß1 increased the expression of TSPAN4 which results in migrasome production. Migrasomes can be internalized by RPE and increase the migration and proliferation ability of RPE. Moreover, TSPAN4-inhibited RPE cells are with reduced ability of initiating experimental PVR. Mechanically, TSPAN4 expression and migrasome production are induced through TGF-ß1/Smad2/3 signaling pathway. CONCLUSION: In conclusion, migrasomes can be produced by RPE under PVR microenvironment. Migrasomes play a pivotal role in RPE activation and PVR progression. Thus, targeting TSPAN4 or blocking migrasome formation might be a new therapeutic method against PVR.

CXCL1 promotes the proliferation of neural stem cells by stimulating the generation of reactive oxygen species in APP/PS1 mice.

PURPOSE: Elevated levels of CXCL1 were observed in the cerebrospinal fluid of patients with early Alzheimer's disease, which may affect neural stem cells in the subventricular zone. We used APP/PS1 mice and neural stem cells to elucidate the role of CXCL1 in Alzheimer's disease. METHODS & RESULTS: We detected CXCL1 in cerebrospinal fluid (CSF), activated macrophages, and microglia suggesting that macrophages may contribute to elevated CXCL1 in the CSF of middle-aged APP/PS1 mice. Proliferation and differentiation of neural stem cells were further analyzed and the results suggested that CXCL1 promotes the proliferation of neural stem cells and inhibits their differentiation into astrocytes. In order to determine how CXCL1 exerts these effects, we analyzed intracellular reactive oxygen species, cell signaling, and performed in vivo recovery experiments. Our results suggest that CXCL1 promotes neural stem cell proliferation through a mechanism involving the production of reactive oxygen species and the PI3K/Akt pathway. CONCLUSION: In APP/PS1 mice, macrophage-derived CXCL1 can promote the proliferation of neural stem cells in the subventricular zone via the NOX2-ROS-PI3K/Akt pathway.

FOXO regulates cell fate specification of Drosophila ventral olfactory projection neurons.

Diverse types of neurons must be specified in the developing brain to form the functional neural circuits that are necessary for the execution of daily tasks. Here, we describe the participation of Forkhead box class O (FOXO) in cell fate specification of a small subset of Drosophila ventral olfactory projection neurons (vPNs). Using the two-color labeling system, twin-spot MARCM, we determined the temporal birth order of each vPN type, and this characterization served as a foundation to investigate regulators of cell fate specification. Flies deficient for chinmo, a known temporal cell fate regulator, exhibited a partial loss of vPNs, suggesting that the gene plays a complex role in specifying vPN cell fate and is not the only regulator of this process. Interestingly, loss of foxo function resulted in the precocious appearance of late-born vPNs in place of early-born vPNs, whereas overexpression of constitutively active FOXO caused late-born vPNs to take on a morphology reminiscent of earlier born vPNs. Taken together, these data suggest that FOXO temporally regulates vPN cell fate specification. The comprehensive identification of molecules that regulate neuronal fate specification promises to provide a better understanding of the mechanisms governing the formation of functional brain tissue.

Activation of brain endothelium by Escherichia coli K1 virulence factor cglD promotes polymorphonuclear leukocyte transendothelial migration.

Escherichia coli K1 is the most common Gram-negative bacteria causing neonatal meningitis. Polymorphonuclear leukocyte (PMN) transmigration across the blood-brain barrier (BBB) is the hallmark of bacterial meningitis. Reportedly, the deletion of virulence factor cglD (E44:ΔcglD) from E44 is responsible for a less efficient PMN transendothelial migration ability. In the present study, we found that complementation of the cglD gene into E44:ΔcglD mutant strain might restore the PMN count and myeloperoxidase level in a neonatal mouse meningitis. Using human brain microvascular endothelial cells (HBMECs), the main model of the BBB in vitro, we found that E44:ΔcglD mutant strain induced a less efficient PMN adhesion to HBMECs and down-regulated chemokines CXCL1, CXCL6 and CXCL8 and adhesion molecule E-selectin, compared with the E44 strain. Complementation of cglD restored the PMN adhesion to HBMECs and the level of these proteins. E44:ΔcglD mutant strain also induced a less efficient NF-κB pathway activation in HBMECs and reduced the soluble p65 (sp65) level in the cerebral spinal fluid of newborn mice, compared with the E44 strain. Complementation of cglD restored the NF-κB pathway activation and increased the sp65 levels. This suggests that cglD in E44 contributes to NF-κB pathway activation in the brain endothelium to promote PMN adhesion to HBMECs and transendothelial migration. Our identified novel requirement of cglD for immune activation and subsequent PMN entry into the central nervous system suggests that therapies directed at neutralising this molecule will be beneficial in preventing bacterial meningitis progression.

Alas1 is essential for neutrophil maturation in zebrafish.

Neutrophils play essential roles in innate immunity and are the first responders to kill foreign micro-organisms, a function that partially depends on their granule content. The complicated regulatory network of neutrophil development and maturation remains largely unknown. Here we utilized neutrophil-deficient zebrafish to identify a novel role of Alas1, a heme biosynthesis pathway enzyme, in neutrophil development. We showed that Alas1-deficient zebrafish exhibited proper neutrophil initiation, but further neutrophil maturation was blocked due to heme deficiency, with lipid storage and granule formation deficiencies, and loss of heme-dependent granule protein activities. Consequently, Alas1-deficient zebrafish showed impaired bactericidal ability and augmented inflammatory responses when challenged with Escherichia coli These findings demonstrate the important role of Alas1 in regulating neutrophil maturation and physiological function through the heme. Our study provides an in vivo model of Alas1 deficiency and may be useful to evaluate the progression of heme-related disorders in order to facilitate the development of drugs and treatment strategies for these diseases.

Magnetic porous carbon derived from Co-doped metal-organic frameworks for the magnetic solid-phase extraction of endocrine disrupting chemicals.

Metal-organic frameworks-5 (MOF-5) was explored as a template to prepare porous carbon due to its high surface area, large pore volume, and permanent nanoscale porosity. Magnetic porous carbon, Co@MOF-5-C, was fabricated by the one-step direct carbonization of Co-doped MOF-5. After carbonization, the magnetic cobalt nanoparticles are well dispersed in the porous carbon matrix, and Co@MOF-5-C displays strong magnetism (with the saturation magnetization intensity of 70.17emu/g), high-specific surface area, and large pore volume. To evaluate its extraction performance, the Co@MOF-5-C was applied as an adsorbent for the magnetic solid-phase extraction of endocrine disrupting chemicals, followed by their analysis with high-performance liquid chromatography. The developed method exhibits a good linear response in the range of 0.5-100 ng/mL for pond water and 1.0-100 ng/mL for juice samples. The limits of detection (S/N = 3) for the analytes were in the range of 0.1-0.2 ng/mL.

Atg7 Regulates Brain Angiogenesis via NF-κB-Dependent IL-6 Production.

The formation of brain vasculature is an essential step during central nervous system development. The molecular mechanism underlying brain angiogenesis remains incompletely understood. The role of Atg7, an autophagy-related protein, in brain angiogenesis was investigated in this study. We found that the microvessel density in mice brains with endothelial-specific knockout of Atg7 (Atg7 EKO) was significantly decreased compared to wild-type control. Consistently, in vitro angiogenesis assays showed that Atg7 knockdown impaired angiogenesis in brain microvascular endothelial cells. Further results indicated that knockdown of Atg7 reduced interleukin-6 (IL-6) expression in brain microvascular endothelial cells, which is mediated by NF-κB-dependent transcriptional control. Interestingly, exogenous IL-6 restored the impaired angiogenesis and reduced cell motility caused by Atg7 knockdown. These results demonstrated that Atg7 has proangiogenic activity in brain angiogenesis which is mediated by IL-6 production in a NF-κB-dependent manner.

Melatonin induces apoptosis of colorectal cancer cells through HDAC4 nuclear import mediated by CaMKII inactivation.

Melatonin induces apoptosis in many different cancer cell lines, including colorectal cancer. However, the precise mechanisms involved remain largely unresolved. In this study, we provide evidence to reveal a new mechanism by which melatonin induces apoptosis of colorectal cancer LoVo cells. Melatonin at pharmacological concentrations significantly suppressed cell proliferation and induced apoptosis in a dose-dependent manner. The observed apoptosis was accompanied by the melatonin-induced dephosphorylation and nuclear import of histone deacetylase 4 (HDAC4). Pretreatment with a HDAC4-specific siRNA effectively attenuated the melatonin-induced apoptosis, indicating that nuclear localization of HDAC4 is required for melatonin-induced apoptosis. Moreover, constitutively active Ca(2+) /calmodulin-dependent protein kinase II alpha (CaMKIIα) abrogated the melatonin-induced HDAC4 nuclear import and apoptosis of LoVo cells. Furthermore, melatonin decreased H3 acetylation on bcl-2 promoter, leading to a reduction of bcl-2 expression, whereas constitutively active CaMKIIα(T286D) or HDAC4-specific siRNA abrogated the effect of melatonin. In conclusion, the present study provides evidence that melatonin-induced apoptosis in colorectal cancer LoVo cells largely depends on the nuclear import of HDAC4 and subsequent H3 deacetylation via the inactivation of CaMKIIα.

Visual Interpretation of Radiomics Features in Filtered Computed Tomography Images during the Portal Phase of Acute Pancreatitis.

BACKGROUND: Current research on radiomics for diagnosing and prognosing acute pancreatitis predominantly revolves around model development and testing. However, there is a notable absence of ongoing interpretation and analysis regarding the physical significance of these models and features. Additionally, there is a lack of extensive exploration of visual information within the images. This limitation hinders the broad applicability of radiomics findings. This study aims to address this gap by specifically analyzing filtered Computed Tomography (CT) image features of acute pancreatitis to identify meaningful visual markers in the pancreas and peripancreatic area. METHODS: Numerous filtered CT images were obtained through pyradiomics. The window width and window level were fine-tuned to emphasize the pancreas and peripancreatic regions. Subsequently, the LightGBM algorithm was employed to conduct an embedded feature screening, followed by statistical analysis to identify features with statistical significance (p-value < 0.01). Within the purview of the study, for each filtering method, features of high importance to the preceding prediction model were incorporated into the analysis. The image visual markers were then systematically sought in reverse, and their medical interpretation was undertaken to a certain extent. RESULTS: In Laplacian of Gaussian filtered images within the pancreatic region, severe acute pancreatitis (SAP) exhibited fewer small areas with repetitive greyscale patterns. Conversely, in the peripancreatic region, SAP displayed greater irregularity in both area size and the distribution of greyscale levels. In logarithmic images, SAP demonstrated reduced low greyscale connectivity in the pancreatic region, while showcasing a higher average variation in greyscale between two adjacent pixels in the peripancreatic region. Moreover, in gradient images, SAP presented with decreased repetition of two adjacent pixel greyscales within the pancreatic region, juxtaposed with an increased inhomogeneity in the size of the same greyscale region within the δ range in the peripancreatic region. CONCLUSIONS: Various filtered images convey distinct physical significance and properties. The selection of the appropriate filtered image, contingent upon the characteristics of the Region of Interest (ROI), enables a more comprehensive capture of the heterogeneity of the disease.

Arctium lappa L. polysaccharides enhanced the therapeutic effects of nasal ectomesenchymal stem cells against liver fibrosis by inhibiting the Wnt/ß-catenin pathway.

The oxidative microenvironment in fibrotic livers often diminishes the effectiveness of mesenchymal stem cells (MSCs)-based therapy. Recent research suggests that pharmacological pre-treatment could enhance the therapeutic performance of MSCs. In this study, we assessed the impact of Arctium lappa L. polysaccharides (ALP) on the biological properties of nasal ectomesenchymal stem cells (EMSCs) and investigated the augmenting effect of ALP pretreatment on EMSCs (ALP-EMSCs) for the treatment of liver fibrosis. ALP treatment demonstrated multiple biological impacts on EMSC functions regarding liver fibrosis: firstly, it maintained the stemness of the cells while boosting the EMSCs' paracrine effects; secondly, it increased the expression of anti-inflammatory and antioxidant factors; thirdly, it inhibited the activation of hepatic stellate cells (HSCs) and liver collagen build-up by modulating the Wnt/ß-catenin signaling pathways. Collectively, these effects helped to halt the progression of liver fibrosis. Therefore, the use of ALP-EMSCs presents an innovative and promising approach for treating hepatic fibrosis in clinical scenarios.

Histone methyltransferase SETD2 is required for proper hippocampal lamination and neuronal maturation.

Proper formation of the hippocampus is crucial for the brain to execute memory and learning functions. However, many questions remain regarding how pyramidal neurons (PNs) of the hippocampus mature and precisely position. Here we revealed that Setd2, the methyltransferase for histone 3 lysine 36 trimethylation (H3K36me3), is essential for the precise localization and maturation of PNs in the hippocampal CA1. The ablation of Setd2 in neural progenitors leads to irregular lamination of the CA1 and increased numbers of PNs in the stratum oriens. Setd2 deletion in postmitotic neurons causes mislocalization and immaturity of CA1 PNs. Transcriptome analyses revealed that SETD2 maintains the expressions of clustered protocadherin (cPcdh) genes. Together, Setd2 is required for proper hippocampal lamination and maturation of CA1 PNs.

Endothelial lincRNA-p21 alleviates cerebral ischemia/reperfusion injury by maintaining blood-brain barrier integrity.

Blood-brain barrier (BBB) disruption is increasingly recognized as an early contributor to the pathophysiology of cerebral ischemia/reperfusion (I/R) injury, and is also a key event in triggering secondary damage to the central nervous system. Recently, long non-coding RNA (lncRNA) have been found to be associated with ischemic stroke. However, the roles of lncRNA in BBB homeostasis remain largely unknown. Here, we report that long intergenic non-coding RNA-p21 (lincRNA-p21) was the most significantly down-regulated lncRNA in human brain microvascular endothelial cells (HBMECs) after oxygen and glucose deprivation/reoxygenation (OGD/R) treatment among candidate lncRNA, which were both sensitive to hypoxia and involved in atherosclerosis. Exogenous brain-endothelium-specific overexpression of lincRNA-p21 could alleviate BBB disruption, diminish infarction volume and attenuate motor function deficits in middle cerebral artery occlusion/reperfusion (MCAO/R) mice. Further results showed that lincRNA-p21 was critical to maintain BBB integrity by inhibiting the degradation of junction proteins under MCAO/R and OGD/R conditions. Specifically, lincRNA-p21 could inhibit autophagy-dependent degradation of occludin by activating PI3K/AKT/mTOR signaling pathway. Besides, lincRNA-p21 could inhibit VE-cadherin degradation by binding with miR-101-3p. Together, we identify that lincRNA-p21 is critical for BBB integrity maintenance, and endothelial lincRNA-p21 overexpression could alleviate cerebral I/R injury in mice, pointing to a potential strategy to treat cerebral I/R injury.

Early prediction of acute pancreatitis severity based on changes in pancreatic and peripancreatic computed tomography radiomics nomogram.

Background: Early identification of severe acute pancreatitis (SAP) is key to reducing mortality and improving prognosis. We aimed to establish a radiomics model and nomogram for early prediction of acute pancreatitis (AP) severity based on contrast-enhanced computed tomography (CT) images. Methods: We retrospectively analyzed 215 patients with first-episode AP, including 141 in the training cohort (87 men and 54 women, mean age 51.37±16.09 years) and 74 in the test cohort (40 men and 34 women, mean age 55.49±17.83 years). Radiomics features were extracted from portal venous phase images based on pancreatic and peripancreatic regions. The light gradient boosting machine (LightGBM) algorithm was used for feature selection, a logistic regression (LR) model was established and trained by 10-fold cross-validation, and a nomogram was established based on the best features. The model's predictive performance was evaluated according to the area under the curve (AUC) of the receiver operating characteristic (ROC) curve, sensitivity, specificity, and accuracy. Results: A total of 13 optimal radiomics features were selected by LightGBM for LR model building. The AUC of the radiomics (LR) model was 0.992 [95% confidence interval (CI): 0.963-0.996] in the training cohort, 0.965 (95% CI: 0.924-0.981) in the validation cohort, and 0.894 (95% CI: 0.789-0.966) in the test cohort. The sensitivity was 0.862 (95% CI: 0.674-0.954), the specificity was 0.800 (95% CI: 0.649-0.899), and the accuracy was 0.824 (95% CI: 0.720-0.919). The nomogram based on the 13 radiomics features showed that SAP would be predicted when the total score was greater than 124. Conclusions: The radiomics model based on enhanced-CT images of pancreatic and peripancreatic regions performed well in the early prediction of AP severity. The nomogram based on selected radiomics features could provide a reference for AP clinical assessment.

Arctium lappa L. root polysaccharides ameliorate CCl4-induced acute liver injury by suppressing oxidative stress, inflammation and apoptosis.

In this study, water-soluble polysaccharides purified from burdock root were used to intervene in carbon tetrachloride (CCl4)-induced acute liver injury (ALI) of BRL3A hepatocytes and rats. Our results indicated that CCl4 significantly inhibited hepatocyte viability and upregulated the expression of reactive oxygen species (ROS), malondialdehyde (MDA), pro-inflammatory cytokines (TNF-α, IL-1ß, and IL-6), and the pro-apoptotic protein Bax. However, Arctium lappa L. root polysaccharides (ALP) could effectively ameliorate liver function and histopathology, oxidative stress, and inflammatory markers. In addition, ALP reduced the expression of apoptotic markers and promoted the proliferation of damaged hepatocytes. In conclusion, ALP possesses a hepatoprotective effect mediated by attenuating oxidative damage, inflammation and apoptosis in ALI.

Preventive Effect of Arctium lappa Polysaccharides on Acute Lung Injury through Anti-Inflammatory and Antioxidant Activities.

The objective of this study was to investigate the preventive effects of polysaccharides extracted from the roots of Arctium lappa (ALP) against acute lung injury (ALI) models induced by lipopolysaccharide (LPS). The polysaccharides were extracted and characterized, and their anti-inflammatory and antioxidant capacities were assessed. The findings demonstrated that ALP could mitigate the infiltration of inflammatory cells and reduce alveolar collapse in LPS-induced ALI in mice. The expression levels of the pro-inflammatory factor TNF-α decreased, while the anti-inflammatory factor IL-10 increased. Furthermore, the administration of ALP improved the activities of lung antioxidant enzymes, including SOD, GSH, and CAT, and lowered MDA levels. These results suggest that ALP exhibits a preventive effect on ALI and has potential as an alternative treatment for lung injury.