22 results about "Mouse Lung" patented technology

This invention relates to the application of β-sitosterol glycoside in the preparation of products for treating lung cancer. This invention creatively provides a new use for the active monomer β-sitosterol glycoside, demonstrating that β-sitosterol glycoside can significantly inhibit the migration ability of lung cancer cells at doses without cell proliferation inhibitors, clarifying the specificity of its anti-metastatic effect, and laying the foundation for further new drug development of this monomer component. Through an in vivo mouse lung metastasis model, this invention demonstrates that β-sitosterol glycoside effectively inhibits the formation of lung metastases while exhibiting no significant toxic side effects in experimental animals, demonstrating high safety, and providing a new candidate molecule for the development of low-toxicity, highly effective anti-lung cancer metastasis drugs.

This invention belongs to the field of biomedical technology and discloses the application of KDELR3 inhibitors in the preparation of drugs for the prevention and / or treatment of individual fibrotic diseases. In a wild-type mouse model of pulmonary fibrosis, compared with the control group receiving intratracheal injection of Scr siRNA, intratracheal injection of KDELR3 siRNA significantly reduced the degree of fibrosis in the mouse lung tissue. KDELR3 inhibition significantly reduced collagen deposition and improved lung tissue structural damage. Further mechanistic studies showed that KDELR3 inhibitors can inhibit the differentiation of fibroblasts into myofibroblasts, thereby reducing the production of fibrosis-related extracellular matrix. These results indicate that KDELR3 is a key molecule regulating the occurrence and development of fibrosis, and drugs that can inhibit KDELR3 expression or activity can be used to prevent and treat various fibrotic diseases, including pulmonary fibrosis, laying the foundation for the development of novel drugs that are effective and safe in treating fibrotic diseases.

The application provides a method for constructing a mouse emphysema model and application, and the method comprises specifically knocking out a PHLDA1 gene in type II alveolar epithelial cells in lung tissue of an animal. Compared with a traditional method for establishing an animal mouse emphysema model by exposing to cigarette smoke, the mouse emphysema model has good stability, can be bred, has a short modeling cycle, and better simulates the lung tissue pathological changes and pathophysiological changes of emphysema patients, and has high consistency with the patients.

The application discloses application of a PRMT3 inhibitor SGC707 in preparation of a drug for treating pulmonary fibrosis, and for the first time verifies that a selective PRMT3 inhibitor SGC707 can dose-dependently inhibit expression of fibrosis markers such as COL1A1 and alpha-SMA in fibroblasts induced by TGF-beta 1 in vitro; in a bleomycin (BLM) induced mouse pulmonary fibrosis model, SGC707 administration can significantly improve lung tissue collagen deposition, reduce inflammatory cell infiltration, repair alveolar structure damage, and effectively down-regulate expression levels of fibrosis related proteins in lung tissues. It is proved that PRMT3 is a functional target with important intervention value in pulmonary fibrosis, SGC707 has definite anti-pulmonary fibrosis activity in vitro and in vivo, and a new drug strategy is provided for treatment of pulmonary fibrosis.

The present application relates to the technical field of content detection, in particular to a method for rapidly detecting the content of hydroxyproline in mouse lung tissue, which comprises the following steps: obtaining the original sampling spectrum of the lung tissue of the mouse to be detected at different preset sampling points, and obtaining a non-lung tissue interference characteristic base matrix containing whole blood characteristics and cartilage characteristics; setting an orthogonal filter operator and determining a lung interstitium characteristic spectrum vector; constructing a reference spectrum vector and determining a relative spectral response factor; constructing a spectral minimum spanning tree and determining a signal contribution weight based on the spectral minimum spanning tree and the relative spectral response factor; generating a whole lung fibrosis synthetic spectrum according to the signal contribution weight and the lung interstitium characteristic spectrum vector, and detecting the content of hydroxyproline based on the whole lung fibrosis synthetic spectrum. The present application considers the non-lung tissue interference containing whole blood characteristics and cartilage characteristics when detecting the content of hydroxyproline, which improves the rationality of the detection of the content of hydroxyproline to a certain extent.

The application discloses a new use of a BET inhibitor YD-851 or a pharmaceutically acceptable salt thereof in the preparation of a drug for treating pulmonary fibrosis. The application finds that YD-851 can inhibit the expression of BRD4 and fibrosis-related markers in pulmonary fibrosis tissues, reduce the structural damage of bleomycin-induced mouse lung tissues, inflammatory cell infiltration and fibrosis pathological changes, and improve lung function damage. Experimental results show that YD-851 can reduce the pulmonary fibrosis score, inflammation score and area ratio of consolidation, improve the lung imaging abnormalities, and down-regulate the expression of fibrosis-related genes such as Col1a1, Fn1 and Acta2. It is shown that YD-851 has the effect of treating pulmonary fibrosis, and can be used for preparing a drug for treating pulmonary fibrosis, and a new use of YD-851 is developed.

The application belongs to the technical field of medicine, and discloses application of a perilla leaf extract in preparation of a medicine for treating and / or preventing asthma-chronic obstructive pulmonary disease (ACO). The perilla leaf extract has a significant curative effect in treating and / or preventing ACO disease, can significantly improve aggregation of inflammatory cells in the lung of an ACO mouse and generation levels of inflammatory factors, and improve lung function and pathological changes of lung tissue inflammation; in addition, the perilla leaf extract can significantly inhibit generation of neutrophil inflammatory factors TNF-alpha, IL-6 and IL-1beta, and inhibit generation of an eosinophil inflammatory factor TNF-alpha.

This invention discloses the application of a peptide SRD in the preparation of drugs for treating acute lung injury, belonging to the field of biomedical technology. In vivo experiments verified the protective effect of peptide SRD on acute lung injury (ALI), particularly its effect on improving AT2 mitochondrial function. In animal models of ALI, tail vein injection of peptide SRD significantly reduced the protein concentration and total cell count in bronchoalveolar lavage fluid, significantly alleviated the severity of lung injury, lowered histological scores, significantly decreased SOD2 acetylation levels while significantly increasing total SOD2 protein levels, and significantly increased SPC levels (an indicator of AT2 survival). ELISA analysis showed a significant decrease in the levels of IL-6, IL-1β, and TNF-α, indicators of pneumonia in mice. These experimental results confirm that the antioxidant peptide SRD can improve oxidative stress damage in ALI, effectively reduce AT2 cell damage under ALI conditions, promote AT2 regeneration and repair, effectively improve lung function, and reduce the inflammatory response of damaged lungs, thus exhibiting a good therapeutic effect on ALI.

This invention relates to the application of mitochondrial formulations in the preparation of drugs for treating chronic obstructive pulmonary disease (COPD). The mitochondrial formulations contain active mitochondria isolated from healthy donor cells, with a particle size of 400–1000 nm, possessing normal mitochondrial membrane potential and ATP generation function, and capable of being internalized by mammalian COPD lung epithelial cells. In vitro cell experiments have confirmed that this mitochondrial formulation can repair CSE-induced mitochondrial dysfunction in lung epithelial cells, inhibit mPTP opening, reduce mtDNA leakage into the cytoplasm, thereby blocking the activation of the cGAS-STING signaling pathway and reducing the release of inflammatory factors such as IL-1β and TNF-α. In vivo experiments in COPD mouse models show that tail vein injection of the mitochondrial formulation can effectively accumulate in lung tissue, significantly improving lung pathological changes such as emphysema and collagen fiber deposition in model mice. This invention provides a novel strategy for COPD treatment based on repairing mitochondrial function and intervening in inflammatory signaling pathways.

The application discloses application of gentisic acid and pharmaceutically acceptable salts thereof in preparation of a medicine for treating pulmonary fibrosis. A large number of experiments show that gentisic acid has obvious effects of inhibiting extracellular matrix deposition, and has certain improvement effects on pulmonary fibrosis tissues of a mouse induced by bleomycin, especially can delay alveolar damage and destruction of lung tissue structure of the mouse with pulmonary fibrosis, so that the application has great application prospects in treatment of fibrosis diseases.

This invention relates to a mitochondrial composite nanosystem DTPS@Mito targeting lung inflammation, comprising a mitochondrial core and a functionalized lipid material DSPE-TK-PEG2000-SA modified on its surface. DSPE acts as a hydrophobic anchor inserted into the mitochondrial outer membrane, PEG2000 provides hydrophilicity and biocompatibility, ketithiothiol bonds serve as ROS-responsive linkers, and sialic acid targets the head group to specifically bind to E-selectin, which is highly expressed at the inflammatory site. The DTPS@Mito particles have a diameter of approximately 832 nm, maintaining intact mitochondrial morphology and protein composition. In vitro experiments show that it significantly inhibits the expression of inflammatory factors, reduces ROS levels, restores ATP production, and regulates mitochondrial dynamics. In vivo experiments show that it has enhanced retention and accumulation capacity in the lungs of ARDS mice, significantly alleviating lung inflammation, tissue damage, and oxidative stress, and reducing hyaline membrane formation. This invention achieves the synergistic integration of three major functions: mitochondrial transplantation, targeted delivery, and antioxidation, and can be used to prepare drugs for the treatment of acute respiratory distress syndrome.

The application provides a novel biphenyl compound and application thereof in preparation of a drug for treating pulmonary fibrosis, relates to the technical field of medicines, and the biphenyl compound is shown as general formula I. The compound can significantly improve BLM-induced pulmonary fibrosis in mice, and specific performance is as follows: reducing the range of pulmonary consolidation, repairing lung tissue structure, improving the survival rate of mice, reducing the lung coefficient, reducing pulmonary interstitial thickening, inflammatory cell infiltration and fibroblast focus formation, reducing abnormal deposition of collagen fibers in the pulmonary interstitium, and having a clear dose-effect relationship and good biological safety. The application provides a solid experimental basis for the application of the compound in preparation of the drug for treating pulmonary fibrosis, and has a wide application prospect.

The utility model discloses a kind of experimental mouse alveolus lavage devices, including the fixing platform for fixing mouse, the syringe for providing lavage liquid, the lavage needle for implementing lavage, the lavage needle fixing joint detachably connected with lavage needle, and the hose of connecting syringe and lavage needle fixing joint;Hose is equipped with hose fixing component, hose fixing component has two mutually parallel fixed surfaces, hose hole is opened on hose fixing component, for hose passes through, the outer wall of hose is fixedly connected with the inner wall of hose hole;Fixing platform is equipped with hose fixing mechanism, and hose fixing mechanism includes fixed frame and binding bolt with the thread connection of fixed frame, two fixed surfaces are respectively matched with the inner wall of fixed frame and the end of binding bolt.The utility model is fixed through the hose fixing component arranged on hose and the hose fixing mechanism arranged on fixing platform in the process of lavage, the fixing of hose and lavage needle, it is convenient for user operation.

This invention belongs to the field of targeted drug technology, and specifically relates to the application of PRDX3 protein as a drug target in screening drugs for the prevention and / or treatment of COPD induced by cigarette smoke. This invention demonstrates that the expression level of PRDX3 protein is increased in COPD mouse models and in cigarette smoke-induced MLE-12 alveolar epithelial cells, and also explores the effect of PRDX3 on COPD disease progression. Overexpression of PRDX3 in alveolar epithelial cells significantly improves lung function and lung tissue damage in COPD mice, while knockdown of PRDX3 exacerbates COPD symptoms in COPD mice. This invention provides a novel drug target and candidate compound for the treatment of COPD, and has significant clinical application value.

The application discloses a human rhubarb extract with anti-influenza A virus activity and a preparation method thereof. The preparation method comprises the following steps: preparing the human rhubarb by fermenting licorice with an artificial synthetic flora (15 kinds of probiotics are mixed according to a specific ratio), and then performing ultrasonic extraction with water as a solvent; and the optimized extraction conditions are as follows: a solid-liquid ratio of 1:30 g / mL, an ultrasonic power of 500 W, an ultrasonic temperature of 50 DEG C, an ultrasonic time of 35 min, and an extraction frequency of 2 times. Compared with traditional extraction and decoction methods, the extract yield is higher, the inhibitory effect on H1N1 influenza A virus is significantly enhanced, the blood clotting titer of mouse lung tissue is reduced to 0.6+ / -0.4, and is equivalent to that of the positive drug oseltamivir phosphate. The application avoids the risk of pathogenic microorganism pollution in traditional pit fermentation, simplifies the medication mode, realizes the reduction and efficiency increase, the process is stable and controllable, is suitable for industrial production, and provides technical support for modern anti-influenza application of the human rhubarb.

This invention relates to extracellular vesicles derived from human mesenchymal stem cells and their use. The extracellular vesicles derived from mesenchymal stem cells according to the present invention inhibit the expression of fibrosis-related proteins, wound closure, and cell infiltration, which are increased in lung epithelial cells due to TGF-β1 treatment. In addition, microRNAs contained in large quantities in the extracellular vesicles inhibit the gene expression of fibrosis-related proteins in lung epithelial cells and lung fibroblasts. These extracellular vesicles significantly reduce the expression of fibrosis-related proteins, collagen production, and fibrotic areas in a mouse model of pulmonary fibrosis. Therefore, the extracellular vesicles according to the present invention can be used to prevent and treat pulmonary fibrosis.

This application discloses a method for monitoring and assessing the replication of Wenzhou-related virus (WZRV) infection based on mouse lung and / or kidney organoids. The method includes: obtaining lung and / or kidney organoids from SD rats; infecting the organoids with WZRV; culturing the infected organoids; and collecting samples at different time points after infection for viral replication and tissue tropism analysis. This application establishes a standardized lung / kidney organoid model from SD rats and, combined with multi-dimensional detection methods such as RT-qPCR nucleic acid quantification, infectivity titer determination, immunofluorescence co-localization, and transmission electron microscopy, can systematically assess viral replication kinetics, tissue / cell tropism, and morphogenesis characteristics. This application constructs a reproducible and comparable standardized assessment system that realistically reflects the replication behavior and target cell preference of WZRV under near-physiological conditions, providing a reliable in vitro platform for viral pathogenesis research and antiviral drug screening.

This invention discloses the application of a sulfonamide derivative in the preparation of a drug for treating respiratory syncytial virus (RSV) pneumonia, belonging to the field of biomedical technology. This invention is the first to discover that 3-(4-methoxyphenyl)-N-[4-[(4-methylpyrimidin-2-yl)sulfonylmethyl]alanine has significant anti-RSV activity, effectively reducing the lung index in RSV-infected mice, improving the pathological lesions in the lungs and bronchi of mice, and significantly reducing the expression of RSV viral load in mouse lung tissue, demonstrating a clear therapeutic effect on RSV-induced pneumonia in mice. This not only provides a novel application direction and experimental evidence for 3-(4-methoxyphenyl)-N-[4-[(4-methylpyrimidin-2-yl)sulfonylmethyl]alanine, but also provides a new and effective candidate drug for the clinical treatment of RSV pneumonia, possessing significant biomedical application value.

The application relates to application of a peppermint-derived exosome in preparation of a medicine for treating LPS-induced ARDS, and the peppermint-derived exosome is obtained through treatment such as soaking in a PBS solution, wall breaking, differential centrifugation, filtration, ultracentrifugation, sucrose density gradient centrifugation and the like. The peppermint-derived exosome in the application can not only reduce histological damage of lung tissue of LPS-induced ARDS mice, improve pulmonary edema, but also has an anti-inflammatory effect on the lung of the ARDS mice, so that the peppermint-derived exosome can be used for preparing a medicine for treating LPS-induced ARDS.

The application belongs to the technical field of biological medicine, and discloses a cyclic antibacterial peptide CycP-1 targeting multi-drug resistant Klebsiella pneumoniae, a composition and application thereof. The amino acid sequence of the antibacterial peptide is shown in SEQ ID NO. 1, the first and the 24th cysteine residues in the molecule form a disulfide bond, and the antibacterial peptide shows a good in-vitro protease stability in a cyclic conformation. Experiments show that the antibacterial peptide has a significant inhibitory effect on multi-drug resistant and pan-drug resistant Klebsiella pneumoniae, and the antibacterial effect can be enhanced, the drug resistance can be reversed or reduced, and the generation of drug resistance can be delayed when the antibacterial peptide is combined with antibiotics. In-vivo experiments of a mouse pneumonia model further prove that after oral administration of the antibacterial peptide, the bacterial load in the lung tissue of a mouse infected with pan-drug resistant Klebsiella pneumoniae can be significantly reduced, the pathological damage in the lung can be reduced, and the survival rate of the infected mouse can be significantly improved, and the effect is better when the antibacterial peptide is combined with polymyxin B.

This invention provides an application of a drug to inhibit silicosis fibrosis. This invention demonstrates that rhodioloside can inhibit the expression levels of fibrosis-related proteins Collagen 1 and α-SMA in SiO2-exposed mice, reduce the number of diffuse high-density shadows and characteristic silicotic nodules in the interstitial lung fields, and decrease the area of ​​diffuse collagen fiber deposition. Simultaneously, rhodioloside can also inhibit TGF-β-induced expression levels of Collagen 1 and α-SMA in NIH / 3T3 cells, inhibiting the transdifferentiation of fibroblasts into myofibroblasts. Furthermore, the research results show that the effect of the same dose of rhodioloside is comparable to, or even superior to, the current first-line clinical drug for alleviating silicosis fibrosis, tetrandrine. These research results prove that rhodioloside can effectively alleviate silicosis fibrosis.