Pan Zhao

Lung injury is a pathological condition caused by a range of direct or indirect factors that disrupt the alveolar-capillary barrier and damage the structure of the lung parenchyma, leading to impaired gas exchange and compromised respiratory function. Lung injury shows a high incidence worldwide and remains associated with high mortality, and safe, effective, and reliable therapeutic strategies for this condition are still lacking. Tetrahedral framework nucleic acids (tFNAs) represent a significant advancement in nucleic acid nanotechnology. As novel therapeutic agents and nanocarriers, tFNAs possess an intrinsic capacity to scavenge reactive oxygen species, thus mitigating oxidative stress. Additionally, their unique tetrahedral geometry facilitates endocytosis-mediated cellular uptake and confers them with excellent tissue permeability, enabling them to traverse the lung mucosal barrier. These properties collectively enhance cell–drug interactions. As a result, tFNAs show multidimensional therapeutic potential for the treatment of lung injuries and provide innovative strategies for managing complex pathological conditions. This review summarizes the recent advances in the application of tFNAs for lung injury repair, with a focus on their mechanisms of action, treatment strategies, and current challenges. The goal of this review is to promote breakthroughs in lung injury treatment. This infographic illustrates all aspects of tetrahedral framework nucleic acid (tFNA) in lung injury treatment. The upper left part, “Intelligent Design of tFNA”, covers responses to ROS, miRNA, pH, and enzymes, which trigger drug release. The upper right part, “Challenges Faced by tFNA”, lists objectives, biosafety, and high cost. The lower right part, “tFNA as Delivery Carrier”, highlights cantilever, sequence replacement, mosaic, and vertex. The lower left part, “tFNA as a Drug”, emphasizes anti-inflammatory effects on macrophages (M1 to M2), ROS neutralization, immune regulation of T cells, and tissue repair. At the bottom, the advantages of tFNA include biodegradability, programmability, cell uptake, and tissue permeability.An infographic on the design, challenges, advantages and applications of tFNAs in the treatment of lung injury.

This study aims to investigate the action mechanism of guaijaverin on pancreatic lipase from multiple perspectives and provide a theoretical basis for the search for new pancreatic lipase inhibitors. The inhibition of pancreatic lipase by guaijaverin was investigated through enzyme inhibition activity experiments, and the IC₅₀ was calculated to determine the type of inhibition of guaijaverin. The mechanism of action was studied by measuring fluorescence, ultraviolet spectra, and circular dichroism. Molecular docking technology was used to explore the binding situation. In addition, in vivo oral lipid tolerance tests in rats were carried out to investigate the inhibitory effect of guaijaverin on pancreatic lipase. Guaijaverin inhibited pancreatic lipase up to 90.63%, confirming its excellent inhibitory ability. The inhibition type was noncompetitive inhibition in reversible inhibition. The multispectral experiments indicated that its quenching type was static quenching and guaijaverin changed the microenvironment and spatial conformation of pancreatic lipase. The molecular docking results showed that the minimum binding energy between the two compounds was −6.96 kcal/mol. In vivo experiments demonstrated that guaijaverin inhibits pancreatic lipase by reducing TG uptake in the body. Guaijaverin has excellent inhibitory effects on pancreatic lipase and has the potential to function as a pancreatic lipase inhibitor.

Isovitexin is a main natural flavonoid component in various plants. Currently, the inhibitory effect of isovitexin on pancreatic lipase (PL) and its mechanism have not been elucidated yet. In the present study, we investigated the inhibitory effect of isovitexin on PL, as well as its interaction mechanism, using enzyme inhibition methods, spectroscopic analysis, and molecular simulations. Results showed that isovitexin possessed significant PL inhibitory activity, with IC₅₀ values of 0.26 ± 0.02 mM. The interaction between isovitexin and PL was dominated by static quenching, and mainly through hydrogen bonding and hydrophobic interaction forces. Analysis of fluorescence spectroscopy confirmed that isovitexin binding altered the conformation of the PL. Circular dichroism (CD) spectrum indicated that isovitexin altered the secondary structure of PL by decreasing the α‐helix content and increasing the β‐fold content. Molecular simulations further characterize the conformational changes produced by the interaction between isovitexin with PL. The performed study may provide a new insight into the inhibitory mechanism of isovitexin as a novel PL inhibitor.

In the numerical calculation process of electromagnetic-thermal bidirectional coupling of permanent magnet synchronous motor (PMSM), as the temperature increases, the residual magnetism and coercive force of the PM gradually decrease, which leads to weakening of the magnetic field and further leads to electromagnetic (EM) torque decreasing in numerical calculation. However, the temperature rise caused by EM torque decreasing is not considered in numerical calculation process, which leads to weaker electromagnetic field and smaller motor loss than those of actual values. Therefore, the calculated temperature in motor is inaccurate. To solve this issue, a control method is proposed to keep the torque as a constant value during numerical calculation process to improve the accuracy of the numerical results of electromagnetic-thermal bidirectional coupling method.

The objective of this study was to investigate the effects and molecular mechanisms of total flavonoids from Cortex Juglandis Mandshuricae (TFC) on preventing alcohol-induced chronic liver injury and regulating gut microbiota in mice. The results showed that oral administration of TFC significantly attenuated alcoholic liver injury in mice. TFC improved lipid accumulation in mice with chronic alcoholic liver injury through activation of the AMPK/PPARα pathway. In addition, TFC maintained the integrity of the intestinal barrier in alcoholic mice, reducing endotoxin leakage from the intestine and further inhibiting the TLR4/NF-κB inflammatory pathway. More importantly, TFC regulated the intestinal microbiota composition and certain bacteria, including Akkermansia muciniphila, Lactobacillus and others. At the same time, reduced levels of short-chain fatty acids due to alcohol consumption were restored. In summary, TFC upregulated AMPK/PPARα signaling pathway to improve hepatic fat accumulation and oxidative stress; TFC positively regulated intestinal flora composition to reduce intestinal disorders caused by alcohol consumption, and further inhibited alcohol-induced inflammatory responses through the intestinal-liver axis. The above findings may be the mechanism of TFC’s pharmacological effects against alcoholic liver injury.

Background: The incidence of respiratory diseases and the respiratory disease mortality rate have increased in recent years. Recent studies have shown that long non-coding RNA (lncRNA) MALAT1 is involved in various respiratory diseases. In vascular endothelial and cancer cells, MALAT1 expression triggers various changes such as proinflammatory cytokine expression, cancer cell proliferation and metastasis, and increased endothelial cell permeability.Methods: In this review, we performed a relative concentration index (RCI) analysis of the lncRNA database to assess differences in MALAT1 expression in different cell lines and at different locations in the same cell, and summarize the molecular mechanisms of MALAT1 in the pathophysiology of respiratory diseases and its potential therapeutic application in these conditions.Results: MALAT1 plays an important regulatory role in lncRNA with a wide range of effects in respiratory diseases. The available evidence shows that MALAT1 plays an important role in the regulation of multiple respiratory diseases.Conclusion: MALAT1 is an important regulatory biomarker for respiratory disease. Targeting the regulation MALAT1 could have important applications for the future treatment of respiratory diseases.