45 results about "Myofibroblast" patented technology

The embodiment of the invention provides a self-powered microneedle patch for repairing hypertrophic scars as well as a preparation method and application of the self-powered microneedle patch. The self-powered microneedle patch comprises: a friction nano-generator for generating a current; the conductive drug-loaded microneedle patch is connected with the friction nano-generator, and the friction nano-generator is connected with the conductive drug-loaded microneedle patch; the conductive drug-loaded microneedle patch comprises a conductive microneedle patch body and a crosslinked gelatin-crosslinked hyaluronic acid microneedle bearing Sb4. The surface of the conductive micro-needle patch is provided with a metal coating, and the conductive micro-needle patch is used for mediating current generated by the friction nano-generator and applying percutaneous electrical stimulation; the cross-linked gelatin-cross-linked hyaluronic acid microneedle is coated at the tip of the conductive microneedle patch. According to the self-powered microneedle patch provided by the embodiment of the invention, myofibroblasts of hypertrophic scars are transdifferentiated into adipocytes by providing percutaneous electrochemical stimulation, inflammatory factor release is inhibited, and a tissue microenvironment is remodeled, so that the hypertrophic scars are reversed, and skin repair and tissue regeneration are realized.

The application discloses a new application of a JAK inhibitor and a medicine for promoting skin stretch regeneration, and application of the JAK inhibitor in preparation of the medicine for promoting skin stretch regeneration; the medicine for promoting skin stretch regeneration comprises the following components: a JAK inhibitor and a carrier, wherein the carrier comprises sodium hyaluronate and propylene glycol; the application provides a new application of the JAK inhibitor, and the JAK inhibitor can promote skin stretch regeneration, in particular, can promote increase of hair follicle density, increase of epidermis thickness, increase of dermis thickness, reduction of fibrosis degree, reduction of immune infiltration degree and reduction of myofibroblast quantity after skin expansion.

This invention discloses a method for preparing a co-loaded dual-gene targeted delivery system and its application, involving the construction and preparation of a dual-gene (pHNF4α, pFOXA3) delivery system. This delivery system can target myofibroblasts (MFs) and activated hepatic stellate cells (aHSCs) and can be used for gene therapy of liver fibrosis. This invention synthesizes the targeting carrier material PEI. 25K -PEG 2K -pPB, through electrostatic adsorption, combines with pHNF4α and pFOXA3 to form a co-loaded dual-gene targeted delivery system, F4α / A3@PP-pPB. This delivery system, through the targeting group pPB, binds to MFs (metacellular matrix cells) that lead to excessive accumulation of extracellular matrix in fibrotic livers and to PDGFR (polydimethylformamide) highly expressed on the surface of aHSCs. On the one hand, it inhibits the activation of aHSCs; on the other hand, it transdifferentiates MFs into hepatocyte-like cells (iHep). These two modes, while combating liver fibrosis, can also achieve a certain degree of liver function reconstruction through transdifferentiated iHep cells, providing new ideas and methods for the effective treatment of liver fibrosis.

The application relates to the field of biomedical technology, and discloses an application of a GCA-NAb monoclonal antibody in the preparation of a drug for preventing and / or treating pulmonary fibrosis. The application mainly relates to the application of an amino acid sequence of the GCA-NAb monoclonal antibody as shown in SEQ ID No. 2 in the preparation of the drug for preventing and / or treating pulmonary fibrosis. The GCA-NAb monoclonal antibody can significantly improve pulmonary fibrosis, and can prolong the survival cycle of a mouse model, reduce the proportion of TH17 cells in lung tissues, and slow down the progress of pulmonary fibrosis. In addition, the antibody can directly affect the transformation of fibroblasts, inhibit the transformation of the fibroblasts into myofibroblasts, and thus reduce the fibrosis. The GCA-NAb monoclonal antibody has the characteristics of high efficiency and safety.

A modality for preventing or treating fibrotic diseases by identifying a marker protein for myofibroblasts is provided. The present invention relates to prophylactic or therapeutic agents for fibrotic diseases, which contain an inhibitor of GPR176 as an active ingredient.

The invention relates to the technical field of medicines, in particular to a novel medical application of a phosphodiesterase 4B inhibitor namiklast, and particularly relates to an application of namiklast in preparation of a medicine for treating intervertebral disc fibrosis through targeted inhibition of macrophage-myofibroblast transformation.

The invention belongs to the technical field of anti-adhesion materials in biomedical engineering, and relates to an anti-adhesion membrane with coarse structure fibers and a preparation method of the anti-adhesion membrane. The method comprises the following steps: soaking an electrostatic spinning fiber membrane containing a high polymer material and a hydrophilic anti-adhesion component in a treating fluid containing the high polymer material and consisting of a poor solvent and a good solvent for a specific time, rinsing and drying to obtain the anti-adhesion membrane, the swelling ratio of the high polymer material in the treating fluid at 25 DEG C for 10 minutes is 1-10% due to the proportion of the inferior solvent to the benign solvent in the treating fluid. A stable integrated nano shish-kebab structure is formed on the surface of the prepared anti-adhesion membrane fiber, exogenous drugs are not needed, spreading of fibroblasts is limited by means of a physical topological structure, conversion of the fibroblasts to myofibroblasts is blocked, the anti-adhesion effect is good, and biocompatibility is good.

The present application relates to the application of delta-Viniferin in the preparation of drugs for preventing or treating metabolic cardiovascular diseases. Delta-Viniferin can inhibit the expression level of aging and inflammation related genes / proteins of vascular endothelial cells, reduce endothelial dysfunction, and clarify its anti-hypertensive effect. Delta-Viniferin can inhibit the expression level of vascular smooth muscle cell phenotype conversion related genes / proteins, improve the contraction function of vascular smooth muscle, and significantly alleviate the degradation of elastic fibers of the vascular wall and the rupture of the intima of the aortic wall in vivo, and clarify its effect on preventing and treating aortic dissection. Delta-Viniferin can inhibit the expression level of myocardial fibroblast fibrosis related genes / proteins, and clarify its anti-myocardial fibrosis effect. Delta-Viniferin can promote white adipose tissue browning by targeting the SIRT1-FOXO1 axis, increase energy consumption, and clarify its effect on resisting obesity. In summary, the compound delta-Viniferin has the effect of protecting various metabolic cardiovascular diseases, and can be used to prepare drugs for preventing and treating metabolic cardiovascular diseases.

The invention relates to the field of binding molecules comprising at least one single variable antibody domain, targeted at receptors present on myofibroblasts and / or hepatic stellate cells (HSCs). The invention also relates to a binding molecule comprising at least two single variable antibody domains, each targeting a receptor on HSCs and / or on myofibroblasts. The invention further relates to nucleic acids encoding such binding molecules, a host cell for expression of such binding molecules and to methods for preparing such binding molecules. The invention further relates to pharmaceutical compositions that comprise such binding molecule and to uses of such binding molecules and / or compositions, in particular for prophylactic, therapeutic or diagnostic purposes.

The invention belongs to the field of biological medicines, and particularly discloses application of a beta-carbon alkali alkaloid derivative, i.e., senecionone, in preparation of an anti-pulmonary fibrosis medicine, and a series of experiments prove that the senecionone can regulate and control a TGF-beta / SMAD signal channel by inhibiting phosphorylation of SMAD < 2 / 3 >, so that fibroblasts are inhibited from being converted into myofibroblasts, and the anti-pulmonary fibrosis effect is achieved. The generation of extracellular matrix protein COL1 and the like is reduced, so that the pulmonary fibrosis is relieved.

An antifibrotic agent is provided, including a copolymer having a constitutional unit (a) containing an N-acetylglucosamine group and a constitutional unit (b) containing a structure represented by General Formula (b) (provided that a constitutional unit corresponding to the constitutional unit (a) is excluded). In General Formula (b), Yb represents a divalent linking group including an oxygen atom. Rb represents a hydrogen atom or an organic group. * represents a bonding site.

The application belongs to the technical field of biological medicine, and particularly relates to a use of Serpine1 gene as a target in preparation of a drug for preventing or treating myocardial fibrosis. In order to screen key molecules for intervention and regulation of extracellular matrix balance, and provide a basis for development of a drug for preventing or treating myocardial fibrosis, the application determines important functions of Serpine1 in myocardial fibrosis through experiments, and provides a use of Serpine1 gene as a target in preparation of a drug for preventing or treating myocardial fibrosis. The application verifies through experiments that knocking down expression of Serpine1 can improve impaired cardiac systolic function caused by thoracic aortic arch constriction for 4 weeks, reduce myocardial fibrosis, and inhibit activation of myocardial fibroblasts, and can be used for preparation of a drug for preventing or treating myocardial fibrosis, and has important practical significance.

The application belongs to the technical field of biological medicine, and particularly relates to an application of an expression agonist of lncRNA Morrbid in preparation of a drug for delaying heart failure and a pharmaceutical composition. The application first confirms a protective effect of lncRNA Morrbid in heart failure, proves that the lncRNA can significantly inhibit activation of myocardial fibroblasts and collagen deposition, reveals that the lncRNA is involved in regulation of key fibrosis and inflammatory signal pathways, and provides a new molecular intervention target for heart failure.

The present invention relates to a multimodal non-invasive in vivo system and related method for the characterization of the tissue microenvironment. The system comprises: a multispectral imaging (MSI) camera for superficial spectral screening; a multispectral optoacoustic tomography (MSOT) module for dynamic vascular and perfusion analysis; a Mueller Matrix Polarimetry (MMP) module for extracellular matrix anisotropy assessment; a Raman spectroscopy module for molecular fingerprinting of fibroblast-associated proteins; an optical coherence tomography (OCT) module for morphological and stratigraphic evaluation; an optional Elastic Scattering Spectroscopy (ESS) module for subcellular scattering biomarkers; and a diachronic analysis module for longitudinal monitoring. Data are integrated by an artificial intelligence processing unit to generate quantitative biomarkers of vascularization, extracellular matrix features, immune activity (Langerhans cells) and fibroblast phenotype, distinguishing physiological myofibroblasts from CAF. The invention enables non-nvasive, biopsy-free evaluation of scars, melanocytic lesions, tumor stroma, wound healing and surgical site monitoring.

The invention provides application of a TP receptor inhibitor in preparation of a medicine for treating cardiac fibrosis, and relates to the technical field of biomedicine. According to the application, the key effect of the TP receptor in heart Gli1 + cells is defined, the TP receptor is determined as an anti-fibrosis specific drug target, and the limitation of insufficient targeting of the existing therapy is broken through. By inhibiting a TP receptor, an AMPK signal channel can be effectively activated, and then ubiquitination degradation of a fibrosis-promoting key factor Gli1 protein is promoted, so that generation and activation of myofibroblasts are inhibited from the source, and the fibrosis process is accurately intervened.

The present invention pertains to combination comprising a CD63-binding molecule and a drug and / or a tracer for use in a method of therapy and / or in a method of in-vivo diagnosis, wherein the drug and / or the tracer is delivered to a myofibroblast.

The present disclosure relates to a use of M-CSF or G-CSF for diagnosis or treatment of pulmonary fibrosis and, more specifically, to: a marker for diagnosing the level of development or progression of pulmonary fibrosis, comprising M-CSF and / or G-CSF; and a composition for preventing or treating pulmonary fibrosis, comprising an M-CSF inhibitor and a G-CSF inhibitor as active ingredients.The present inventors have ascertained that M-CSF and / or G-CSF is a marker for development or progression of pulmonary fibrosis, and have confirmed that a composition, which comprises M-CSF and G-CSF and which binds to M-CSF and G-CSF so that the inherent mechanism thereof can be prevented, has an effect of significantly inhibiting myofibroblast hyperplasia or pulmonary fibrosis of the pulmonary cells, and thus the marker and the composition of the present disclosure are expected to be effectively usable for diagnosis, prevention or treatment of pulmonary fibrosis.

The application discloses application of a cytokine interleukin-17D (IL-17D) in preparation of a medicine for preventing and / or treating scars. IL-17D is highly expressed in fibroblasts, but is down-regulated in myofibroblasts in skin scars and keloids. Low expression of IL-17D makes IL-17D unable to inhibit expression of fibrosis-related genes, thus unable to inhibit differentiation of fibroblasts into myofibroblasts, thereby causing generation of scars. Overexpression of IL-17D or injection of recombinant IL-17D protein in a mouse full-thickness skin wound can significantly inhibit formation of scars; after IL-17D gene of the mouse is knocked out, expression of fibrosis-related genes in the skin wound is up-regulated, and scars after wound healing are obviously aggravated. Therefore, the application discloses that IL-17D can be used as a medicine for diagnosing and treating skin scars or keloids.

This invention discloses a combination of biomarkers, a kit, and their applications for detecting hypertrophic scars (HTS). The biomarker combination includes a core biomarker and / or auxiliary biomarker 1 and / or auxiliary biomarker 2; the core biomarker is ABCC9 and CSPG4, auxiliary biomarker 1 is RGS5 and ACTA2, and auxiliary biomarker 2 is PDGFRB and TRPC6. This invention also provides a kit containing the above biomarker combination detection reagents and a drug screening method. This invention reveals for the first time that pathological pericytes are the core fibrotic cells in HTS, breaking through the traditional understanding that fibroblasts are the dominant cells. By targeting and inhibiting the abnormal activation, proliferation, and transdifferentiation of pericytes into myofibroblasts, the generation of myofibroblasts and matrix deposition are curbed at the source, providing a new strategy for precision treatment of HTS. Compared with traditional therapies, this approach has higher specificity and can achieve early molecular warning and quantitative detection of trace tissues for HTS, effectively overcoming the lag and subjectivity of clinical morphological diagnosis.

The invention discloses application of obakunone in preparation of a medicine for preventing and treating myocardial infarction and myocardial fibrosis. A myocardial infarction animal model is constructed, the specific mechanism of obakunone for improving fibrosis is explored in vivo, meanwhile, a cell model for converting macrophages into myofibroblasts (MMT) is constructed in vitro, and research finds that obakunone can inhibit the MMT process. The research results provide a medicine for preventing and treating myocardial infarction and myocardial fibrosis, which has a good application prospect.

Disclosed is an artificial scaffold material for a wound applied to the wound in order to cure the wound while suppressing scarring in a living body. The scaffold material includes: a biomaterial having a property to which progenitor cells of myofibroblasts of the living body adhere; and an anti-fibrotic agent contained and retained in the biomaterial, the anti-fibrotic agent being gradually released from the biomaterial as the biomaterial dissolves in the living body. The wound includes at least one of an open wound and a closed wound in the living body. The anti-fibrotic agent has a low molecular weight, and inhibits the progenitor cells from differentiating into the myofibroblasts in the living body. The scaffold material for a wound is placed on a target surface of at least one of the wound surface of the open wound, the wound surface of the closed wound, and a portion of the surface of the living body where the closed wound is exposed, thereby allowing the anti-fibrotic agent to be locally administered to the target surface.

The present invention relates to an immune sensitivity identification and regulation method based on the expression association of DUSP11 and nc886, and more specifically, to a method for providing immune response information, the method comprising a step for measuring the expression levels of DUSP11 and nc886. In the present invention, it was found that nc886 and DUSP11 are negatively correlated, and nc886 increases according to DUSP11 depletion in various cell types (epithelial cells, fibroblasts, and myofibroblasts). In addition, it was found that vtRNA in the 5'-PPP form increases upon depletion of DUSP11, thereby increasing immune response, but nc886 (vtRNA2-1) in the 5'-P form increases due to DUSP11 depletion, thereby decreasing immune response. That is, in the present invention, it was found that when the expression of nc886 in the 5'-P form increases as a result of DUSP11 depletion, inflammatory responses caused by IFN are alleviated due to the increased 5'-P-nc886, and thus the present invention can be used as a method for providing information on immune status using the correlation between nc886 and DUSP11.

This invention relates to the pharmaceutical field, specifically to a drug for the prevention or treatment of endometrial fibrosis, comprising poloxamer and spermidine; poloxamer is added to the spermidine solution and swelled at 3-5°C until completely dissolved to form a liquid precursor; the liquid precursor undergoes a phase transition at 35-40°C to form a gel; the liquid precursor is injected into the uterine cavity to reduce the expression of αSMA in the endometrial tissue, inhibit the transformation of stromal cells into myofibroblasts, and promote angiogenesis.

The invention discloses application of flueggeine B or pharmaceutically acceptable salt thereof in preparation of a medicine for treating pulmonary fibrosis. The chemical structure of the flueggeine B is shown as a formula (I). The flueggemine B shows an improvement effect in a bleomycin-induced pulmonary fibrosis mouse model, improves the weight and lung function parameters of a mouse, relieves the degree of pulmonary fibrosis, has an inhibition effect on lung tissue collagen deposition, can also effectively improve the phenotype of pulmonary epithelial cells and inhibit abnormal activation of myofibroblasts, and can be used for treating pulmonary fibrosis. Therefore, the traditional Chinese medicine composition has a remarkable relieving effect on bleomycin-induced pulmonary fibrosis.

This invention discloses the application of NLRX1 protein inhibitors in the preparation of products with protective effects against pulmonary fibrosis, belonging to the field of biomedical technology. This invention, through the use of an NLRX1 gene knockout mouse model and siRNA silencing technology, demonstrates that inhibiting NLRX1 can significantly alleviate bleomycin-induced pulmonary fibrosis pathological damage. Its protective mechanisms include promoting the proliferation of type II alveolar epithelial cells, inhibiting their damage and apoptosis, and reducing myofibroblast infiltration and extracellular matrix deposition. Based on this, this invention provides for the first time a therapeutic strategy targeting the inhibition of the NLRX1 protein. Related products include recombinant vectors containing RNA molecules encoding NLRX1 expression inhibitors or other drugs capable of inhibiting NLRX1 expression. This invention provides new targets and drug development directions for the treatment of fibrotic diseases, especially pulmonary fibrosis.

The invention discloses a nano preparation for treating pulmonary fibrosis and a preparation method thereof, and belongs to the technical field of biological medicines. The nano preparation is a double-nanoparticle preparation and comprises a nanoparticle A targeting far-end airway epithelial cells and a nanoparticle B targeting myofibroblasts, the nanoparticle A is prepared from PLGA (poly (lactic-co-glycolic acid))-PEG (polyethylene glycol), PLGA-PEG-HA (hyaluronic acid) and a notch inhibitor; the nanoparticle B is prepared from PLGA (poly (lactic-co-glycolic acid)-PEG (polyethylene glycol), PLGA-PEG-Mal (poly (lactic-co-glycolic acid)-PEG-Mal), a peptide of a targeted myofibroblast and a Hedgehog inhibitor. According to the nano preparation disclosed by the invention, the airway progenitor cells are jointly regulated and controlled to differentiate to the alveolar lineage through the double nanoparticles, so that the treatment of pulmonary fibrosis is realized.

To provide a technique for suppressing excessive scarring of a biological tissue in a wound healing process.SOLUTION: An artificial scaffold material for wound applied to wound of a living body contains a biological absorbing biomaterial and an anti-fibrosis agent as main components, wherein the biomaterial contains the anti-fibrosis agent at least during usage of the scaffold material for wound. The biomaterial functions as an artificial extracellular matrix having properties to bond a precursor cell of a myofibroblast of a living body, in a wound. The scaffold material for wound is placed in an abdominal cavity so that at least one of a first contact in which it is placed in the wound and / or comes in local contact with a region having a first wound part, out of the inner surface of the abdominal wall of the living body, and a second contact in which it comes in local contact with a region having a second wound part, out of the outer surface of a target organ in the abdominal cavity. Thereby, the anti-fibrosis agent is locally administrated into the wound, and anti-scarring treatment is conducted in a wound healing process.SELECTED DRAWING: Figure 2

To provide a technique for suppressing excessive scarring of a biological tissue in a wound healing process.SOLUTION: An artificial scaffold material for wound applied to wound of a living body contains a biological absorbing biomaterial and an anti-fibrosis agent as main components, wherein the biomaterial contains the anti-fibrosis agent at least during usage of the scaffold material for wound. The biomaterial functions as an artificial extracellular matrix having properties to bond a precursor cell of a myofibroblast of a living body, in a wound. The scaffold material for wound is placed so that it comes in local contact with wound formed on the inner surface of a closed lumen in the living body, during usage. Thereby, the anti-fibrosis agent and the biomaterial are locally administrated into the wound, and thereby in a wound healing process, anti-scarring treatment is conducted in an anti-scarring treatment delaying suppression state.SELECTED DRAWING: Figure 4

The invention relates to an application of Kp1 (at) HCeO2 (at) SAM in preparation of drugs for treating or improving inflammatory bowel diseases, and the Kp1 (at) HCeO2 (at) SAM is prepared by embedding KP1-loaded HCeO2 composite nanoparticles into SAM. The invention further provides the Kp1 (at) HCeO2 (at) SAM for treating or improving the inflammatory bowel disease and a preparation method of the Kp1 (at) HCeO2 (at) SAM. According to the invention, the oral KP1 (at) HCeO2 (at) SAM composite microspheres are constructed, so that the acute inflammatory response of IBD is coordinated and intervened, and the chronic fibrosis process is reversed. In a DSS-induced mouse colitis model, the platform shows a staged curative effect: in an acute inflammation stage, HCeO2 efficiently clears active oxygen, promotes macrophage to be converted into M2 anti-inflammatory phenotype and reduces inflammatory factor expression, so that intestinal barrier function recovery is promoted; in the chronic fibrosis period, the sustained-release KP1 oligopeptide can inhibit a TGF-beta / Smad pathway in a targeted mode, myofibroblast activation and collagen deposition are remarkably inhibited, and therefore intestinal fibrosis lesion is reversed. Therefore, the composite microsphere disclosed by the invention, as a novel oral preparation for treating IBD, shows a wide clinical application prospect.

The application discloses an in-situ self-adhesive anti-fibroin protein colloid cornea and a preparation method and application thereof, and belongs to the field of biomedical polymer materials. With mulberry silk as raw material, degumming and dissolution are carried out to obtain a fibroin protein solution; methacryl modification and o-nitrobenzyl type phototrigger molecule coupling are respectively carried out; after dialysis and freeze-drying, two kinds of sponges are obtained; the two kinds of sponges are dissolved in a phosphate buffer solution containing a photoinitiator, and a pirenfibrate bioactive factor is added to obtain a precursor solution. The precursor solution is added dropwise to a corneal lamellar stroma defect, and after ultraviolet light irradiation, the colloid is rapidly cross-linked in-situ. The colloid cornea realizes suture-free adhesion by forming a chemical bond on a wet surface through an o-nitrobenzyl group, and inhibits the formation of corneal myofibroblasts to resist fibrosis through pirenfibrate. The light transmittance, burst pressure and adhesion force of the colloid cornea can be adjusted, the biocompatibility is excellent, the corneal stroma regeneration can be promoted, and the risk of scar formation can be reduced, so that the colloid cornea has important clinical application value.