62 results about "Alveolar epithelial cell" patented technology

The invention belongs to the technical field of biological medicine manufacturing, and particularly provides a preparation method of an engineered exosome capable of loading mitochondria for treating pulmonary fibrosis and the engineered exosome. The method comprises the following steps: constructing fusion plasmids for expressing mitochondrial targeting peptide fragment-therapeutic protein genes, dissolving the fusion plasmids in non-enzyme ultrapure water, adding the fusion plasmids into a lipid nano-preparation, and fully mixing to obtain a nano-preparation containing the therapeutic protein genes; the nano preparation is delivered into alveolar epithelial cells and is efficiently transfected, so that the homeostatic balance of the injured alveolar epithelial cells in the development of pulmonary fibrosis is effectively regulated and controlled, the secretion of an exosome with a therapeutic effect is promoted, and the engineered exosome is further obtained through mannose modification. The exosome can effectively load mitochondria and sequentially and accurately target macrophage mitochondria on the basis of a mannose target head and a mitochondrial targeting peptide fragment, so that macrophage mitochondrial homeostatic balance is effectively regulated and controlled, the purpose of reverse treatment of pulmonary fibrosis is achieved, and the exosome has high clinical application value.

The invention relates to the technical field of organoid culture, in particular to a pulmonary fibrosis organoid model and a construction method and application thereof. The pulmonary fibrosis organ-like model is obtained by co-culturing lentivirus stably transfected alveolar epithelial cells, human embryonic lung fibroblasts MRC-5 and macrophages. According to the invention, macrophages are innovatively introduced, a ternary co-culture system of lentivirus stably transfected alveolar epithelial cells, human embryonic lung fibroblasts MRC-5 and macrophages is constructed, and a key'epithelial injury-immune infiltration-fibroblast activation 'pathological triangle in a pulmonary fibrosis pathogenesis process can be more comprehensively simulated; the finally obtained pulmonary fibrosis organ-like model provides an efficient tool for pulmonary fibrosis mechanism research and research, development and screening of anti-pulmonary fibrosis drugs.

The application discloses use of LncRNA00_178, miR-466b-3p and Gucy1b1 as acute lung injury markers or drug targets, and belongs to the technical field of biomarkers and drug targets. LncRNA00_178 can be used as a biomarker for screening or diagnosing acute lung injury, a miR-466b-3p down-regulator can be used to prepare a pharmaceutical composition for preventing and treating acute lung injury, and Gucy1b1 can be used as a drug target to prepare a drug for preventing and / or treating acute lung injury. The application has the beneficial effects that the application proposes that LncRNA00_178 and miR-466b-3p, and miR-466b-3p and Gucy1b1 have a target binding relationship. LncRNA00_178 can be used as a biomarker for screening or diagnosing acute lung injury, the silence of miR-466b-3p inhibits LPS-induced apoptosis of alveolar epithelial cells, and Gucy1b1 can be used as a drug target to prepare a drug for preventing and / or treating acute lung injury. The data provide new insights for the treatment mechanism of ALI and the identification of specific targets, and provide a new idea for the research and development of new drugs for acute lung injury, and have a wide application prospect.

The invention discloses a transrespiratory tract noninvasive drug delivery carrier and a preparation method and application thereof.The transrespiratory tract noninvasive drug delivery carrier comprises a lipid bimolecular layer and bioactive ingredients wrapped in the lipid bimolecular layer, and the lipid bimolecular layer comprises a liposome membrane and an enzyme responsive modification part embedded into the liposome membrane; the enzyme responsive modification part is a substrate polypeptide capable of being degraded by RTC-enz and polyethylene glycol connected with the substrate polypeptide. According to the invention, an enzyme-responsive modification part is introduced to the surface of a liposome membrane, so that efficient targeted disintegration of the liposome membrane is realized in pulmonary alveoli in an RTC-enz environment. Bioactive components carried by the liposome are uniformly distributed on the surface of a'gas-blood barrier 'in the pulmonary alveolus after the liposome is disintegrated, so that effective retention and uniform dispersion can be realized, and the condition that the liposome which cannot be disintegrated blocks a'gas-liquid' barrier on the surface of the pulmonary alveolus at the end of the respiratory tract is avoided; and potential toxicity caused by transfection of bioactive components carried by liposome which cannot be disintegrated into alveolar epithelial cells is also avoided.

The invention discloses a construction method and application of a human lung 3D cell microsphere and a human pulmonary fibrosis 3D organoid. The construction of the human lung 3D cell microspheres comprises the following steps: respectively digesting human primary fibrosis cells and human II-type alveolar epithelial cells which are subjected to adherent culture into single cells; mixing digested human primary fibrotic cells, human II-type alveolar epithelial cells and THP-1 macrophages subjected to suspension culture according to a cell number ratio of 1: 1: 1, so as to obtain a cell precipitate; and preparing the cell precipitate into cell matrigel microspheres by using a T-type microfluidic technology, and culturing to obtain the human lung 3D cell microspheres. And further inducing the human lung 3D cell microspheres by using a human lung organoid culture medium containing 50ng / mL of TGF-beta for 24-48 hours to obtain the human pulmonary fibrosis 3D organoid. According to the invention, 3D cell microspheres with human normal lung cell characteristics and protein expression can be formed within 3 days, and pulmonary fibrosis 3D organs can be obtained after short-time induction.

The invention provides a lung-kidney interaction simulation system based on an organ chip, and the system comprises a lung chip module which is used for simulating a qi-blood barrier structure of a lung, and the lung chip module is inoculated with human alveolar epithelial cells and human lung microvascular endothelial cells; the kidney chip module is used for simulating a capillary lumen of a kidney tubule and a kidney tubule lumen structure, and human kidney tubule epithelial cells and human umbilical vein endothelial cells are inoculated on the kidney chip module; the connecting channel is used for communicating the lung chip module with the kidney chip module and allowing the culture medium to flow between the lung chip module and the kidney chip module; and wherein a klebsiella pneumoniae liquid for causing lung injury is applied to the upper layer of the lung chip module. The invention provides a novel simulation system for the research of lung-kidney interaction, and solves the limitation of animal experiments.

Provided is a pharmaceutical for lung regeneration, the pharmaceutical containing vascular endothelial stem cells. Also provided is a method for producing an alveolar organoid, the method comprising a step for three-dimensional co-culture of vascular endothelial stem cells and alveolar epithelial cells. This pharmaceutical for lung regeneration is useful in the treatment of lung disease accompanied by alveolar damage, such as chronic obstructive lung diseases, infectious lung diseases, and pulmonary fibrosis.

Provided is an RNA editing system activating a Wnt signaling pathway, relating to the field of gene editing. Provided is an RNA editing element, comprising an Axin1-targeting RNA fragment and an Axin2-targeting RNA fragment. A gRNA that targets both Axin1 and Axin2 is constructed, which, compared with gRNAs targeting Axin1 or Axin2 alone, can significantly up-regulate Wnt activity. An AAV6 vector is screened from three AAV vectors of different serotypes, and exhibits relatively high expression intensity and efficiency and high infection efficiency with respect to airway epithelial cells and alveolar epithelial cells while exhibiting very low infection efficiency with respect to immune cells and endothelial cells. The AAV vector is assembled with a Cre-LoxP recombinase system to together infect a host cell, thereby facilitating the measurement of Cas13d knockdown efficiency by means of fluorescent labeling.

The invention belongs to the technical field of biological materials, and particularly relates to a pathogen-targeted engineered exosome as well as a preparation method and application thereof. The engineered exosome provided by the invention comprises an adipose-derived stromal cell exosome, antibacterial peptide M27-39 and 6 '-sialic acid lactose, and integrates two functions of resisting influenza virus and relieving viral pneumonia, targeted modification of 6'-SL can simulate a host receptor structure, and binding of HA and sialic acid is competitively blocked. After the antibacterial peptide M27-39 carried by the exosome is released in the lung, the direct antiviral effect can be achieved, excessive inflammatory response induced by viruses is inhibited, and meanwhile lung injury caused by influenza virus infection is relieved by promoting alveolar epithelial cell repair and relieving pathological injury of viral pneumonia. Therefore, the engineered exosome provided by the invention can be combined with pathogenic microorganisms in a targeted manner, and has obvious functions of resisting pathogenic microorganisms, resisting inflammation, repairing barriers and intervening the pathological process of infectious lung injury.

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 invention belongs to the technical field of medical biological research, and particularly relates to a construction method of a spontaneous emphysema mouse model. The invention relates to a method for constructing a spontaneous emphysema mouse model, which comprises the following steps: when a Muc1 gene whole body knockout mouse naturally senility for 3-18 months to form spontaneous emphysema and / or a Muc1 type 2 alveolar epithelial cell knockout mouse is 6-8 weeks old, injecting tamoxifen into the intraperitoneal cavity of the mouse to induce knockout. According to the invention, the Muc1 gene knockout mouse is used for constructing a spontaneous emphysema mouse model product for the first time; the related products comprise construction schemes, application transformation and the like of a spontaneous emphysema model generated by Muc1 whole body knockout mouse (Muc1- / -) along with age increase and a spontaneous emphysema model generated by Muc1 type 2 alveolar epithelial cell knockout (Muc1AT2- / -) mouse induced by intraperitoneal injection tamoxifen along with age increase. The invention proves that the spontaneous emphysema model is successfully constructed.

The invention relates to the technical field of biological medicines, in particular to application of palmitic acid and a preparation thereof in preparation of medicines for preventing and treating acute exacerbation of chronic obstructive pulmonary diseases. The invention provides application of palmitic acid and a preparation thereof in preparation of a medicine for preventing and treating acute exacerbation of chronic obstructive pulmonary disease. Research finds that supplement of palmitic acid in an acute infection period can improve IFITM3 protein expression of alveolar epithelial cells and further promote downstream secretion of TGF beta by up-regulating the expression level of anti-inflammatory cytokines, so that lung tissue inflammation regression and tissue repair are promoted, and the lung function of patients with chronic obstructive pulmonary diseases is improved.

The invention discloses an application of targeted METTL15 in preparation of a protection preparation for treating plateau pulmonary edema, which aims at reducing the injury effect of alveolar epithelial cells induced under an anoxic condition under the condition of intervention of caffeine; for the METTL15 knockout alveolar epithelial cells, the hypoxia protection effect of the caffeine disappears, the caffeine can act on the METTL15 to play a role in enhancing the mitochondrial function so as to play a protection role in the hypoxia-induced alveolar epithelial cells, and the caffeine acts on the METTL15 and serves as a protection factor for hypoxia injury by maintaining the mitochondrial function so as to play a role in protecting the hypoxia-induced alveolar epithelial cells. The compound has a good application prospect in prevention and treatment of plateau emphysema.

The invention provides a construction method and application of a sepsis model based on a lung and kidney organ chip. The method comprises the following steps: S1, carrying out ultraviolet sterilization on an organ chip device; s2, modifying a transwell plug-in unit; s3, inoculating human lung microvascular endothelial cells and human umbilical vein endothelial cells; S4, inoculating human alveolar epithelial cells and human renal tubular epithelial cells; s5, transwell inserts are arranged in two holes in the middle of the organ chip device respectively, a mixed culture medium is added into liquid adding holes in the two sides of the organ chip device, and the lung chip and the kidney chip are communicated through a lower channel of the organ chip device; s6, dynamically culturing the lung and kidney organ chip; and S7, sucking up the culture medium in the constructed lung and kidney organ chip, adding the LPS-containing mixed culture medium into a lower channel, and respectively adding the LPS-containing mixed culture medium into the human alveolar epithelial cell side and the human renal tubular epithelial cell side of the lung and kidney organ chip and the transwell plug-in hole for culturing for 2 days. According to the invention, the lung and kidney organ chip is applied to the sepsis model for the first time, and the constructed sepsis model is more suitable for basic research and drug development of sepsis.

The present invention relates to a novel method of treating pulmonary emphysema in patients suffering from alpha-1 antitrypsin deficiency (AATD), a genetic disorder that causes low levels of alpha-1 antitrypsin (AAT), a protein that protects the lungs from damage by neutrophil elastase. The invention consists of aerosolizing nanoparticles composed of apolipoprotein A1 enriched with AAT (A1NP). The invention aims to deliver these nanoparticles directly to the lungs, where they can interact with the alveolar surface and modulate the inflammatory and proteolytic processes that lead to emphysema. In particular, the inventors report that said nanoparticles are not cytotoxic, have anti-inflammatory and anti-elastase properties, can cross alveolar epithelial cells, and are not immunogenic in mice.

The invention discloses an exosome for treating sepsis lung injury. The research result shows that the HO-1 modified alveolar epithelial cell source exosome is used for performing intervention treatment on lung injury in a CLP model, so that the generation of lung tissue inflammatory factors and pro-inflammatory M1 type macrophages can be remarkably reduced, the inflammatory reaction is reduced, the lung tissue edema exudation and pathological injury degree is reduced, and the sepsis lifetime is prolonged. The HO-1 modified pulmonary alveolar epithelial cell source exosome has important treatment potential on sepsis lung injury, and has good research significance and application prospect.

The invention discloses a novel application of hederagenin in preparation of a medicine for maintaining the dryness of alveolar II epithelial cells, the hederagenin is definitely used for preparing the medicine for maintaining the dryness of the alveolar II epithelial cells for the first time, and the repairing effect of the hederagenin on ATII dry damage is verified through in-vivo and in-vitro experiments. A brand new treatment strategy is provided for lung diseases such as acute lung injury, pulmonary fibrosis and the like which are characterized by ATII dry failure, the technical blank of intervention of natural active ingredients in ATII dry is filled up, a new way which is efficient, low in cost and easy to obtain is provided for ATII dry maintenance, the concentration of a medicine prepared from the natural active ingredients is screened, and the clinical application prospect is wide. An important theoretical basis is provided for further medication and medicine preparation, meanwhile, the pharmacological application range of the hederagenin is expanded, and a new target and a new strategy are provided for subsequent intervention treatment of lung diseases such as acute lung injury and pulmonary fibrosis needing injury repair.

The invention belongs to the technical field of biological medicine, provides novel application of PRMT6, and particularly relates to application of a PRMT6 inhibitor in preparation of a medicine for preventing or treating sepsis-ARDS. The invention discloses the application value of the PRMT6 as the sepsis-ARDS treatment target for the first time. According to the application disclosed by the invention, the expression of PRMT6 is inhibited in a targeted manner, ferroptosis in alveolar epithelial cells (AECs) can be effectively inhibited, and the histopathology related to ARDS is further improved, so that the disease progress is effectively improved, and a new path is opened up for targeted therapy of sepsis-ARDS.

The invention discloses an exosome composition containing resveratrol, astragalus membranaceus and ginseng as well as a preparation method and application of the exosome composition, and belongs to the technical field of biological medicines. The exosome composition disclosed by the invention is obtained by inducing alveolar epithelial cells by active ingredients containing resveratrol, an astragalus extract and a ginseng extract and then secreting the alveolar epithelial cells. The preparation method of the exosome composition mainly comprises the following steps: co-culturing the active component and alveolar epithelial cells, and then sequentially carrying out differential centrifugation and ultracentrifugation on the collected cell supernatant to purify the exosome. The invention also provides a pharmaceutical preparation containing the exosome composition. According to the composition, traditional Chinese medicine active ingredients are combined with a modern cell exosome technology, a potential strategy is provided for prevention and treatment of pulmonary fibrosis, and the composition has a good application prospect.

The application discloses a method for constructing a cell membrane fusion model induced by a novel coronavirus-like particle, and belongs to the technical field of biology. The method comprises the following steps: constructing a virus-like particle containing a SARS-CoV-2 spike protein gene and an RNA packaging sequence PS9, using HEK-293T cells as packaging cells, co-expressing structural proteins M, E, N and S protein, and realizing assembly of VLPs without replication ability. Subsequently, the VLPs are used to infect immortalized type II alveolar epithelial cells, S protein expression is induced and cell-cell membrane fusion is mediated without the need of BSL-3 laboratory conditions. The formation of fused giant cells can be directly observed through ZO-1 protein immunofluorescence staining, the model is stable, has high biological safety, and is repeatable in vitro. The application overcomes the safety risk of live virus infection and the authenticity problem of a transient transfection model, can be used for research on a SARS-CoV-2 virus membrane fusion mechanism, and has a good application prospect.

The invention belongs to the technical field of medicines, and particularly relates to novel application of polyethylene glycol in preparation of a medicine for treating or reversing pulmonary fibrosis. A new normal form for reversing diseases in a force treatment mode by applying middle-low molecular weight polyethylene glycol (PEG with the molecular weight of 200-3000 Da) to improve extracellular osmotic pressure is put forward and verified for the first time. Through functional verification of cell experiments and animal experiments, the system illustrates that the force treatment activates a mechanical sensitive signal network by inducing alveolar epithelial cell volume compression so as to realize a deep mechanism of EMT (epithelial-mesenchymal transition) molecular cascade reversion. The action path from the physical force to the biological signal provides a brand new theoretical foundation stone for developing a fibrosis treatment strategy based on mechanical microenvironment regulation and control, and PEG300 is a representative preferable embodiment.

The invention discloses application of an MUC1-C segment in preparation of a medicine for preventing or treating chronic obstructive pulmonary disease, and belongs to the technical field of protein functions and targeted medicine development. The MUC1-C protein level in the lung tissue and alveolar epithelial cells of a COPD patient is detected, and cell experiments and animal experiments jointly prove that down-regulation of MUC1-C expression is significantly related to the aging level of the lung tissue, the level of differentiation from AT2 cells to AT1 cells, the inflammation level, mitochondrial dysfunction and reduction of lung functions. MUC1-C overexpression can effectively relieve deterioration of the pathological process. The invention can be applied to the fields of research and development of new drugs and new technologies for diagnosing, preventing and treating chronic obstructive pulmonary disease, and the like.

The invention provides a method for preparing inhalable targeted gold nanoparticles for accelerating pulmonary delivery and treating pulmonary inflammation. The method comprises the following steps: preparing plasmids; carrying out plasmid transformation; carrying out protein expression induction; carrying out protein purification; and the gold nanoparticles (Au (at) PEG-RBD NP) combined with the spikes RBD are prepared. Nanoparticles (NP) in air accumulate more readily in lungs with lipopolysaccharide-induced acute respiratory distress syndrome (ARDS) than in healthy lungs and enter alveolar epithelial cells that express angiotensin converting enzyme (ACE) 2 and L-SIGN (both are Spike receptors activated in ARDS hamsters). The nanoparticles (NP) treat tissue damage, oxidative stress, and inflammation more effectively than corticosteroids, and do not remain gold or create toxicity in the major organs one year after inhalation. The gold core can be used for inhibiting p38 alpha mitogen activated protein kinase and polo-like kinase 3. Similar therapeutic effects have been observed in hamsters suffering from hydrochloric acid induced ARDS. This self-therapeutic nanoparticle (NP), when combined with biomimetic and non-invasive delivery, provides a safe, efficient, and targeted treatment for lung inflammation.

The invention discloses an exosome composition and method for treating lung diseases, and relates to the technical field of medicines.The composition is composed of human alveolar epithelial cell exosome subjected to hypoxia pretreatment, traditional Chinese medicine compound nano-liposome and an atomization stabilizer, the mass ratio of the exosome to the traditional Chinese medicine compound nano-liposome is 1: 1-1: 3, and the mass ratio of the atomization stabilizer to the human alveolar epithelial cell exosome to the traditional Chinese medicine compound nano-liposome is 1: 1-1: 3. The preparation method comprises the steps of cell culture, exosome purification, traditional Chinese medicine liposome preparation and composition mixing treatment, during treatment, an intelligent atomizer can be used for administration, and abdominal respiration training and traditional Chinese medicine iontophoresis therapy are matched. According to the scheme, the targeting property is high, the side effect is small, the inflammatory pathway can be effectively inhibited, the pulmonary epithelium-mesenchymal transition is reversed, the drug delivery efficiency is improved, and the drug delivery system is suitable for treating idiopathic pulmonary fibrosis, acute attack of asthma and the like.

The invention provides a method for constructing an alveolar epithelial cell in-vitro aging model from tobacco tar, and belongs to the technical field of cigarette extracts. The method comprises the following steps: firstly, adding fetal calf serum and penicillin-streptomycin double antibodies into a culture medium to obtain a culture solution, then culturing alveolar epithelial cells in a 5% CO2 cell incubator at 37 DEG C, and inducing by adopting tobacco tar to form an in-vitro aging model. According to the method, the culture mode of the alveolar epithelial cells is adjusted, the tobacco tar is added to stimulate aging, the obtained in-vitro aging model of the alveolar epithelial cells is good in stability and easy to repeat, and the tobacco tar is adopted for induction, so that the in-vitro aging model is closer to an in-vivo real environment.

Disclosed is use of 5α-androst-3β,5,6β-triol or an analogue, a deuterated compound or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for the treatment of a pulmonary disease in a patient. These compounds can significantly inhibit the up-regulation of PFKFB3 expression, significantly inhibit the accumulation of lactate, significantly reduce vascular endothelial cell injury, significantly reduce alveolar epithelial cell injury, significantly inhibit alveolar septum thickening, significantly reduce alveolar damage, and thus can be used to treat diseases mediated by lung epithelial cell injury and / or vascular endothelial cell injury, such as in the lung.

The invention discloses an application of TRAF7 in screening of anti-lung injury drugs. In an LPS-induced A549 cell acute lung injury model, TRAF7 gene knock-down significantly aggravates cell apoptosis and inflammatory response, which shows that inflammatory factor release is increased, and cell injury is aggravated; and TRAF7 overexpression can obviously inhibit the pathological change. The result shows that the TRAF7 has a protection effect on alveolar epithelial cells, the expression level of the TRAF7 is in negative correlation with the in-vitro lung injury degree, and it is proved that the TRAF7 has a negative regulation effect in acute lung injury. In a mouse ALI model, TRAF7 overexpression can significantly reduce the total number of cells, the total protein content and the wet / dry weight ratio of lung tissue in bronchoalveolar lavage fluid (BALF), relieve the pathological injury score of the lung and inhibit LY6Gneutrophil and CD68 macrophage infiltration. The TRAF7 can effectively relieve LPS-induced pulmonary edema, vascular permeability increase and tissue inflammation, and the anti-inflammatory and tissue protection functions of the TRAF7 in an in-vivo model are verified.

The invention relates to the field of biological medicine, in particular to a nano-carrier system targeting aging alveolar epithelial cells as well as preparation and application of the nano-carrier system. The preparation method comprises the following steps: carrying out self-assembly on chemically synthesized PEI-Se-Se-BAI1 and si-cGAS to form BAI1-cGAS particles; the alveolar epithelial cells with high expression of Anti-DPP4-Scfv are obtained through gene editing, and the extracellular vesicles alpha-DPP4-MNs are obtained through centrifugation; finally, the BAI1-cGAS and the alpha-DPP4-MNs are subjected to membrane extrusion, and the nano carrier system BAI1-cGAS (at) DNs is prepared. The nano-carrier system can specifically target aged alveolar epithelial cells in pulmonary fibrosis through Anti-DPP4-Scfv, BAI1 is released, mitochondrial outer membrane permeability is inhibited, and mtDNA is prevented from being released to cytoplasm; meanwhile, si-cGAS is released, and activation of a cGAS / STING pathway and a downstream inflammation pathway is inhibited, so that inflammatory aging of alveolar epithelial cells is resisted, and pulmonary fibrosis is treated. The nano-carrier system integrates the advantages of aging cell membrane positioning, responsive drug release, dual inflammation pathway inhibition and the like, specifically delays the aging of alveolar epithelial cells, and provides an efficient, safe and accessible method for treating pulmonary fibrosis.

The invention belongs to the field of drug activity, and particularly relates to application of dimethyl fumarate in preparation of alveolar cell regeneration drugs. The invention systematically evaluates the effect of dimethyl fumarate in the process of promoting pulmonary alveolar regeneration by constructing a pulmonary alveolar organ model and a bleomycin-induced lung injury mouse model. Research results show that dimethyl fumarate can significantly promote regeneration of alveolar epithelium AT2 cells, so that alveolar epithelium structure repair is accelerated.

The invention provides application of a GSDMD inhibitor in preparation of a chronic obstructive pulmonary disease (COPD) treatment preparation, and relates to the technical field of biological medicines.The COPD mouse model induced by cigarette smoke is established and divided into a control group, a COPD group and a COPD + inhibitor group (GS DMD inhibitor), and the GS DMD inhibitor and the COPD + inhibitor group (GS DMD inhibitor) are combined through methods of Western Blot, ELISA, qPCR, a transmission electron microscope and the like, so that the chronic obstructive pulmonary disease (COPD) treatment preparation is obtained. And detecting GSDMD pathway related protein and gene expression, inflammatory factor release level and alveolar barrier function change. A GSDMD channel in the COPD model group is obviously activated, which shows that the expression levels of GSDMD-N and Caspase-1 are increased; the concentration of IL-1beta and IL-18 is obviously increased; the expression levels of NLRP3, ASC and pro-Caspase-1 and the concentration of HMGB1 in BAL F are increased, the alveolar epithelial cell structure is damaged, and the wet-to-dry ratio and the total protein content are increased. The GSDMD inhibitor significantly reduces the above indexes and improves the airway epithelial barrier function. It is determined that the GSDMD pathway aggravates the airway epithelial cell injury and inflammatory response of COPD by inducing pyroptosis. The GSDMD inhibitor can significantly inhibit pyroptosis and improve COPD-related pathological changes, and provides a new target and theoretical basis for treatment of COPD.