52 results about "CCL2" patented technology

The invention relates to the technical field of biomedicine, in particular to a method for efficiently separating and preparing exosomes, which comprises the following steps: S10, providing human umbilical cord mesenchymal stem cells; s20, culturing the human umbilical cord mesenchymal stem cells by using an exosome induction culture medium; the exosome induction culture medium contains a first inflammatory factor; a second inflammatory factor is added in the culture process; the first inflammatory factor comprises at least one selected from the following groups: IL-6 and TNF-alpha; the second inflammatory factor comprises CCL2; and S30, collecting the supernatant of the culture medium in the step S20, and centrifugally collecting to obtain the exosome. The method can improve the yield of the exosomes, has the advantage of simple operation, is suitable for extracting a large amount of exosomes, and has a good clinical application prospect.

Biomarker-based treatment, monitoring, and diagnostic methods for IL-17 dependent conditions, including hidradenitis suppurativa, are disclosed. The biomarkers may be selected from IL6, PLA2G2A, IL19, P13, CST7, IL17A, IL17F, GH1, MZB1, IL1B, IFNG, TNC, CXCL9, SLAMF7, VEGFA, IL17C, SLAMF1, SDC1, OSM, LBP, REG3A, CD79B, COL4A1, CLEC4D, VWF, IL5RA, CSF3, TGFA, IL2RA, ITIH3, FCAR, CCL23, NRCAM, RETN, SERPINA11, CLEC4G, CSF1, HGF, CRELD2, EFEMP1, LTBR, NME3, CKAP4, CD276, SPON2, GGH, TIMP1, LY9, MCFD2, TCN2, QPCT, HYOU1, TNSFSF13B, CCL2, CCL3, CCL4, CCL5, CCL7, CCL20, CXCL1, CXCL8, PDFGA, CXCR2, CCR6, CXCL13, PCDH1, BOC, MEPE, ADAM 23, THOP1, IL1RL2, RCOR1, EDAR, and combinations thereof. Kits for measuring the biomarkers, diagnosing and treating IL-17-dependent conditions, and identifying super-responders are also disclosed.

The present invention discloses a set of diagnostic markers for aortic dissection and their applications. The markers include the genes MMP8, ALOX15, HP, FXYD2, SIGLEC8, and CCL2. The genes MMP8, ALOX15, HP, FXYD2, SIGLEC8, and CCL2 protected by the present invention can be used as biomarkers for AD and as indicators for assessing disease severity in AD patients, enabling efficient diagnosis of patients with aortic dissection.

The invention discloses CCL2, a receptor specific binding polypeptide thereof and application of the receptor specific binding polypeptide in prevention and treatment of cholestatic liver diseases, and relates to the technical field of biological medicines. The CCL2 and the receptor specific binding polypeptide thereof, which are screened by a molecular simulation technology, can be specifically bound with a key molecule CCL2 for inducing diseases and a plurality of receptors thereof in a cholestatic liver disease occurrence process, so that liver function indexes are recovered; the traditional Chinese medicine composition can be used for relieving liver pathological injury, including inhibiting bile duct hyperplasia, relieving portal vein inflammatory response and relieving portal vein fibrosis, so that the pathological development process of fibrosis and inflammation caused by the liver injury is blocked.

Biomarker-based treatment, monitoring, and diagnostic methods for IL-17 dependent conditions, including hidradenitis suppurativa, are disclosed. The biomarkers may be selected from IL6, PLA2G2A, IL19, PI3, CST7, IL17A, IL17F, GH1, MZB1, IL1B, IFNG, TNC, CXCL9, SLAMF7, VEGFA, IL17C, SLAMF1, SDC1, OSM, LBP, REG3A, CD79B, COL4A1, CLEC4D, VWF, IL5RA, CSF3, TGFA, IL2RA, ITIH3, FCAR, CCL23, NRCAM, RETN, SERPINA11, CLEC4G, CSF1, HGF, CRELD2, EFEMP1, LTBR, NME3, CKAP4, CD276, SPON2, GGH, TIMP1, LY9, MCFD2, TCN2, QPCT, HYOU1, TNSFSF13B, CCL2, CCL3, CCL4, CCL5, CCL7, CCL20, CXCL1, CXCL8, PDFGA, CXCR2, CCR6, CXCL13, PCDH1, BOC, MEPE, ADAM23, THOP1, IL1RL2, RCOR1, EDAR, and combinations thereof. Kits for measuring the biomarkers, diagnosing and treating IL-17-dependent conditions, and identifying super-responders are also disclosed.

This invention relates to the field of biomedical technology, and particularly to the application of crotonin A in the preparation of drugs for treating IgA nephropathy. Pharmacodynamic experiments conducted in vivo on a Thy1 rat model showed that crotonin A effectively reduced 24-hour urinary protein and the urinary protein-to-creatinine ratio in an IgA nephropathy model—an anti-Thy1 rat nephritis model—and inhibited the expression of mRNAs of genes related to renal cortical inflammation, proliferation, and fibrosis, including Cyclin E, α-SMA, FN, CCL2, NF-κB, and IL-6, further improving renal pathology. In in vitro cell models, crotonin A inhibited the proliferation of rat mesangial cells and suppressed the expression of mRNAs of TGF-β, Cyclin E, α-SMA, CCL2, NF-κB, and IL-6, indicating that crotonin A has significant anti-inflammatory, anti-cell proliferation, and anti-fibrotic effects. Brucella oleracea has considerable therapeutic potential, providing a potential new drug option for the clinical prevention and treatment of IgA nephropathy, and is of great significance for the development of safe and effective drugs for the treatment of IgA nephropathy.

The invention relates to a synthesis method of a histone deacetylase 4 small-molecule inhibitor and application of the histone deacetylase 4 small-molecule inhibitor in resisting vascular endothelial aging. A novel HDAC4 small-molecule inhibitor is synthesized by a simple and efficient novel method, and the structural formula of the inhibitor is shown in the specification. The HDAC4 small-molecule inhibitor has strong affinity with HDAC4, can obviously reduce the expression quantity of HADC4 and P21 proteins and mRNA of vascular endothelial cells and the expression quantity of mRNA of inflammation-related proteins Il6, CCL2 and Il-1beta, has an obvious effect of resisting senescence of the vascular endothelial cells, has very good druggability and safety, and can be used for preparing an anti-aging medicine for preventing senescence of the vascular endothelial cells. The compound can be used for preparing medicines for treating vascular endothelial senescence and related diseases thereof. # imgabs0 #

Methods for treating or inhibiting fibrosis in a subject by administering specific chemokine cocktails are described. The chemokine cocktails include combinations of CXCL4, CXCL9, CXCL10, CXCL11 and / or CXCL12 proteins, or the combination of CXCL1 and CXCL8 proteins. Methods for increasing extracellular matrix (ECM) production and / or treating a wound in a subject by administering specific chemokine cocktails are also described. In these methods, the cocktails include CXCL1 and CXCL8 proteins and optionally further include a CCL2 protein.

The invention relates to application of beta-glucan in preparation of a preparation for reducing the expression quantity of related genes of skin extracellular matrix inflammation. The structure of the beta-glucan is formed by connecting structural units. The invention also provides a biomarker, the biomarker is a gene related to skin extracellular matrix inflammation, and the gene comprises any one or a combination of at least two of IL1A, IL1B, IL1R1, IL1RAP, IL6, NFKB2, FOSB, FOSL1, JUN, JUND, CCL2, PTGS2, MMP10, MMP12, MMP13, CXCL8, CD86, PLAU, GADD45A, TNFSF18, TNFRSF10B, TNFRSF12A, TNFRSF14 or TNFRSF21.

The invention relates to an application of an ROS (reactive oxygen species) response type multifunctional nano-delivery drug in preparation of a drug for treating anxiety disorder related to high myopia or high myopia, the drug is TK-F-PEI / siR-A, the drug takes ROS response TK-F-PEI as a carrier, a CCL2 nucleic acid aptamer is arranged on the surface of the carrier, and MMP9siRNA is packaged on the core of the carrier. The invention further provides a preparation method of the medicine. The composition can effectively relieve inflammatory response in high myopia, reduce monocyte infiltration to a central nervous system, target local damaged blood eye and blood brain barriers caused by high myopia through CCL2 / ROS double response, promote barrier repair and break vicious circle of inflammation by silencing MMP9 expression, thereby relieving anxiety symptoms of high myopia patients, and improving the treatment effect of the high myopia patients. The living quality of the patient is improved. The pharmaceutical preparation provided by the invention has the advantages of strong pertinence, obvious curative effect, small side effect and the like, provides a new thought and method for treatment of high myopia related complications, and has a wide application prospect.

The present invention discloses molecular markers for differential diagnosis of aortic dissection and acute myocardial infarction and their applications. The molecular markers include gene SIGLEC8, gene CCL2, gene PRR35, gene FAM240C, gene TNFAIP8L3, and gene ASTL. The genes SIGLEC8, CCL2, PRR35, FAM240C, TNFAIP8L3, and ASTL protected by the present invention can be used as biomarkers for differentiating aortic dissection and acute myocardial infarction. The markers protected by the present invention have the potential for good differential diagnosis of patients with aortic dissection and acute myocardial infarction, and have good diagnostic efficacy, which can distinguish patients with aortic dissection from those with acute myocardial infarction, enabling patients to receive effective treatment in a timely manner.

Biomarker-based treatment, monitoring, and diagnostic methods for IL-17 dependent conditions, including hidradenitis suppurativa, are disclosed. The biomarkers may be selected from IL6, PLA2G2A, IL19, PI3, CST7, IL17A, IL17F, GH1, MZB1, IL1B, IFNG, TNC, CXCL9, SLAMF7, VEGFA, IL17C, SLAMF1, SDC1, OSM, LBP, REG3A, CD79B, COL4A1, CLEC4D, VWF, IL5RA, CSF3, TGFA, IL2RA, ITIH3, FCAR, CCL23, NRCAM, RETN, SERPINA11, CLEC4G, CSF1, HGF, CRELD2, EFEMP1, LTBR, NME3, CKAP4, CD276, SPON2, GGH, TIMP1, LY9, MCFD2, TCN2, QPCT, HYOU1, TNSFSF13B, CCL2, CCL3, CCL4, CCL5, CCL7, CCL20, CXCL1, CXCL8, PDFGA, CXCR2, CCR6, CXCL13, PCDH1, BOC, MEPE, ADAM 23, THOP1, IL1RL2, RCOR1, EDAR, and combinations thereof. Kits for measuring the biomarkers, diagnosing and treating IL-17-dependent conditions, and identifying super-responders are also disclosed.

This invention belongs to the field of medicine, specifically disclosing a drug-loaded biomimetic nanodecoy based on genetic engineering, its preparation method, and its application. The drug-loaded biomimetic nanodecoy of this invention comprises CCR2-overexpressing nanovesicles, and the hydrophobic regions of the nanovesicles are loaded with curcumin. This invention also provides a method for preparing the drug-loaded biomimetic nanodecoy based on genetic engineering and its application. The overexpressed CCR2 is used to adsorb excess CCL2 to inhibit the binding of macrophages to CCL2, preventing macrophage chemotaxis and subsequent TGF-β production. This inhibits the activation of hepatic stellate cells by removing pro-fibrotic mediators upstream; simultaneously, curcumin is released to block the downstream TGF-β / Smad signaling pathway, thereby inhibiting the activation of hepatic stellate cells.

The invention belongs to the technical field of biological medicines, and particularly relates to application of IAA in preparation of a medicine for preventing and treating atherosclerosis. Atherosclerosis is caused by excessive deposition of cholesterol, and IAA can significantly reduce formation of aorta and aortic sinus lipid plaques of atherosclerosis model mice by adjusting monocyte chemotactic and adhesion functions (specifically, down-regulating expression of chemotactic factors CCL2 and CXCL1, receptors CCR1 and CCR2, adhesion molecules ICAM1 and the like). An injection preparation is preferably selected as a medicine dosage form, the intervention dosage of IAA is 50 mg / kg, and the intervention time is 15 weeks. The new application of IAA in prevention and treatment of atherosclerosis is explored for the first time, the action mechanism of IAA is clear, the intervention effect is remarkable, and a new target spot and thought are provided for developing safe and effective medicines and means for preventing and treating atherosclerosis.

The present invention pertains to the use of gene editing and miRNA technologies for improving recombinant production of ANGPTL3 mimetics in CHO cells. The gene expression modifications are used for knock-out / knock-down of the endogenous protein CCL2 of the CHO cells which is difficult to separate from ANGPTL3 mimetics during purification.

This invention discloses a dual-pathway nanoformulation targeting the sclera, its preparation method, and its applications. The nanoformulation uses ketithial-modified fluorinated polyethyleneimine (TK-F-PEI) as a carrier, with a core loaded with hypoxia-inducible factor-1α small interfering RNA (HIF-1α siRNA) and a surface-coupled chemokine CCL2 nucleic acid aptamer. After local ocular administration, this formulation can efficiently target scleral lesions in myopic eyes, neutralizing CCL2 through the aptamer to improve the scleral inflammatory microenvironment, while simultaneously releasing siRNA to silence HIF-1α to inhibit the intracellular hypoxia pathway, synergistically reversing pathological scleral remodeling and delaying axial elongation. This invention's formulation exhibits strong targeting, good safety, and significant efficacy, providing a novel combined targeted drug delivery strategy for the clinical treatment of myopia, especially high myopia.

The invention discloses an application of a CCL2 / CCR2 signal channel blocker in relieving chemotherapeutic drug-induced heart injury, and belongs to the technical field of biological medicines. The invention finds that a CCL2 / CCR2 signal channel blocker, particularly a CCL2 neutralizing antibody, has an obvious effect of improving the chronic cardiotoxicity induced by the chemotherapeutic drug adriamycin, and also can cooperate with the therapeutic effect of the chemotherapeutic drug at the same time. On the basis, the invention provides a combined treatment strategy based on a CCL2 neutralizing antibody, and the cardiotoxicity problem and tumor drug resistance challenge in the clinical application of the adriamycin are solved at the same time through targeted regulation and control of a CCL2 signal channel.

The invention relates to the field of immunology, in particular to preparation of a mucous membrane adjuvant for recruiting pre-DC and application of the mucous membrane adjuvant in influenza vaccines. Tridecafluoroheptyl ethylene oxide and mannose are grafted on polyethyleneimine, the polyethyleneimine and structural protein hemagglutinin of influenza viruses are adsorbed to form a nano vaccine MF25PEI / HA, secretion of CCL2 is promoted by activating a TLR4 pathway of nasal cavity cDC, pre-DC is recruited and differentiated into cDC, and the network steady state of the nasal cavity cDC is maintained. HA uptake is increased by targeting cDC, cDC maturation is stimulated, and high-level immune response is induced. After intranasal immunization of MF25PEI / HA, secretion of high-level IgA and IgG is caused, activation of B cells, T cells and Tfh cells is promoted, and differentiation of memory B cells and memory T cells is induced. Effective protection can be provided for the influenza H1N1 virus, and a new thought is provided for research and development of respiratory mucosa vaccines.

The present invention pertains to the use of gene editing and miRNA technologies for improving recombinant production of ANGPTL3 mimetics in CHO cells. The gene expression modifications are used for knock-out / knock-down of the endogenous protein CCL2 of the CHO cells which is difficult to separate from ANGPTL3 mimetics during purification.

The present application relates to a kind of histone deacetylase 4 small molecule inhibitor synthesis method and the application of anti-vascular endothelial senescence.The present application is synthesized with simple and efficient new method a new HDAC4 small molecule inhibitor, its structural formula is as follows.The HDAC4 small molecule inhibitor has strong affinity with HDAC4, can significantly reduce the expression amount of HADC4 and P21 protein and mRNA of vascular endothelial cell and the mRNA expression amount of inflammation-related protein Il6, CCL2 and Il-1 beta, has the effect of significantly anti-vascular endothelial cell senescence, and has good drug property and safety, can be used for preparing the drug for treating vascular endothelial senescence and its related diseases.

The invention provides preparation of siRNA (small interfering Ribonucleic Acid) targeting CCL2 and application of the siRNA in treating pain, and relates to the technical field of biomedicine, and the technical key points are as follows: a cholesterol methoxy modified siRNA molecule for inhibiting CCL2 gene expression at least comprises one of the following three groups: Ccl2-mous-104, Ccl2-mous-246 and Ccl2-mous-329. The invention provides three groups of siRNA molecules, the three groups of siRNA molecules can obviously reduce CCL2 gene expression in vitro, the three groups of siRNA molecules can effectively reduce CCL2mRNA expression in vitro, and the mRNA level of the Ccl2-mous-246 group is the lowest; based on the data, the Ccl2-mous-246 has the most significant effect of inhibiting CCL2 gene and protein expression, effectively relieves neuropathic pain of mice, and lays a foundation for clinical treatment of pain.

This invention relates to a drug for treating ischemia-reperfusion injury and its application. The drug activates the CCL2-chemokine receptor 2 signaling axis, triggering the downstream G protein αi2 subunit-mediated phosphatidylinositol 3-kinase / protein kinase B signaling pathway. This, in turn, synergistically regulates the antioxidant defense system driven by nuclear factor erythroid 2-related factor 2 and the B-cell lymphoma 2-mediated anti-apoptotic pathway, thereby treating the ischemia-reperfusion injury. The results of this study establish a novel therapeutic strategy for testicular ischemia-reperfusion injury based on engineered exosomes, and simultaneously reveal the previously undiscovered cytoprotective role of the CCL2 / CCR2 signaling axis in non-immune cells.

The invention discloses application of andrographolide and a pharmaceutical composition thereof in preparation of a medicine for preventing and / or treating lung cancer, particularly lung metastatic tumor, and belongs to the technical field of medicine. In-vivo and in-vitro experiments of a system prove that andrographolide can inhibit activation of a nuclear factor kappa B (NF-kappa B) signal channel by down-regulating expression of glycogen synthase kinase 3beta (GSK3beta), and particularly, phosphorylation and nuclear translocation processes of an NF-kappa B p65 subunit Ser536 site are inhibited. According to the effect, transcription and expression of downstream target gene chemotactic factors CCL2 and CXCL1 are effectively reduced, finally, infiltration of tumor-related macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) in tumor tissue is remarkably reduced, aggregation of anti-tumor immune cells such as CD8 + T cells is promoted, an immunosuppressive microenvironment is reversed into an immune activation state, and the immunosuppressive activity of tumor cells is improved. And lung cancer metastasis is inhibited from the source. The invention provides a brand new candidate drug and a clear action mechanism for clinical prevention and treatment of lung cancer metastasis, and has a good development prospect.

This invention relates to the field of biotechnology and discloses a stem cell co-expressing miR-449a-5p and miR-30c-5p. The stem cell is constructed by cloning a biomimetic polycistronic expression cassette containing miR-449a-5p and miR-30c-5p into a lentiviral vector and infecting the stem cell, enabling stable and synergistic expression of these two miRNAs. The exosomes (miRNAs-Exos) secreted by these cells specifically enrich miR-449a-5p and miR-30c-5p; after local administration, the exosomes are taken up by skin cells, and the two miRNAs synergistically inhibit the expression of the aging-associated secretory phenotype (SASP) core factors CCL2 and PAI-1, downregulate matrix metalloproteinases MMP-1 / MMP-3, reduce collagen degradation, improve the dermal inflammatory microenvironment, and thereby promote collagen synthesis and skin barrier repair.

This invention discloses the application of targeting and inhibiting the MSR1-PI3K / AKT signaling pathway in the treatment of kidney injury induced by polylactic acid (PLA) microplastic particles (PLMPs). The study shows that oligomeric PLA MPs recognize and activate the downstream PI3K / AKT signaling pathway via MSR1, significantly upregulating the expression of the chemokine CCL2, thereby amplifying the macrophage-mediated inflammatory cascade. By inhibiting MSR1 or blocking the PI3K / AKT signaling pathway, the macrophage accumulation, inflammation activation, and renal tissue structural damage induced by oligomeric PLA MPs can be significantly reduced, thereby treating PLA MPs-induced kidney injury. This invention reveals for the first time the key regulatory role of the MSR1-PI3K / AKT signaling axis in PLA MPs-induced kidney injury, providing a new molecular target and intervention strategy for the prevention and treatment of degradable MPs-related kidney diseases.

The invention relates to hepatic fibrosis intervention, and provides a pharmaceutical composition for treating and / or preventing hepatic fibrosis related to TET2 function deficiency type myeloid cells and application of the pharmaceutical composition. The composition comprises: (a) an inhibitor or antagonist for inhibiting chemotactic signals mediated by CCL2 and / or CCL8 and CCR2 and / or CCR3; and (b) an IL-6 pathway inhibitor. Preferably, (a) is Bindarit or a pharmaceutically acceptable salt thereof, and (b) is an IL-6 neutralizing antibody or an IL-6 receptor antibody. According to the composition, by reducing mononuclear cell recruitment / proinflammatory mononuclear cell source macrophage infiltration and blocking IL-6 mediated hepatic stellate cell activation, collagen deposition is relieved, and fibrosis indexes such as alpha-SMA and Col1a1 are reduced. Animal experiments show that in a CCl4-induced myeloid Tet2 deletion mouse model and an old-age chimeric model, combined administration is superior to single administration.

The invention relates to a target and a pharmaceutical composition for treating or diagnosing triple negative breast cancer, and relates to the field of biological medicines. The invention further discloses application of the inhibition reagent for the c-Myc / CCL2 signal axis target of the triple negative breast cancer in preparation of drugs for treating the triple negative breast cancer. The c-Myc / CCL2 signal axis target detection reagent for the triple negative breast cancer is applied to preparation of a diagnostic kit for prognosis evaluation of diagnosis of the triple negative breast cancer. By inhibiting the functions of c-Myc or / and CCL2, polarization of M2 type macrophages can be reversed, and an anti-tumor immune microenvironment can be remodeled; meanwhile, c-Myc or / and CCL2 can be used as a biomarker for prognosis evaluation of the triple negative breast cancer. The invention provides a new treatment strategy and diagnostic tool for triple negative breast cancer, and has important clinical application value.

Therapeutic agents and treatment methods for urologic cancers, particularly urologic cancers with reduced lysine (K)-specific demethylase 6A (KDM6A) function, the agents and methods being characterized by suppressing both IL-6 activity and CCR2 / CCL2 activity, are provided.

This invention provides a probe library and kit for detecting genetic risk gene mutations in viral infections, belonging to the field of gene detection technology. The probe library and kit designed in this invention achieve, for the first time, the simultaneous detection of all mutations in the following 51 genetic risk genes for viral infections: CARMIL2, CCL2, CD27, CD70, CIB1, CTPS1, CXCR4, CYBC1(C17orf62), DBR1, FCGR3A, FCHO1, ICAM1, IFIH1, IFNAR1, IFNAR2, IFNGR1, IFNGR2, IL10, IL10RA, IL10RB, IL... The probe library and kit of this invention contain 18BP, IRF3, IRF7, IRF9, MAGT1, LIG1, MCM2, NOS2, OAS1, POLR3A, POLR3C, POLR3F, PRKCD, RASGRP1, SH2D1A, STAT1, STAT2, TBK1, TICAM1, TLR3, TLR7, TLR8, TMC6, TMC8, TNFRSF9, TRAF1, TRAF2, TRAF3, TYK2, UNC93B1, and XIAP. This invention's probe library and kit can be used for detecting genetic variations in the risk of viral infection in clinical settings, assessing an individual's genetic risk of viral infection, and has broad application prospects.

The invention discloses application of lupinone (Lup) in preparation of drugs for preventing or treating depression and anxiety, and belongs to the technical field of application of natural drugs. The results of an open field experiment and an elevated cross maze experiment show that the Lup can effectively improve the depression behavior and the accompanying anxiety behavior of a disease model mouse. Meanwhile, a differential gene protein interaction network is obtained by analyzing a transcriptome of an experimental mouse, and a result shows that gene expressions of Acta2, Fos, Tagln, Vwf, Ccl2 and the like have significant differences and can possibly play key biological functions under experimental conditions, so that valuable clues and directions are provided for subsequent in-depth research, and the application prospect is broad. And further analysis of related biological mechanisms and pathological processes is facilitated. The result shows that Lup has potential treatment value in the aspect of improving depression and anxiety symptoms, and an experimental basis is provided for developing related treatment drugs.