26 results about "CCL2" patented technology

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.

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.

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 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.

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.

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.

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.

The present application provides polyclonal antibodies for alleviating or treating pain in humans or animals, compositions comprising them, and uses thereof. In particular, the invention relates to a yolk IgY polyclonal antibody against pain mediator molecules NGF, CCL2 and CGRP and a composition thereof. The pain phenomenon of the OA sick dog can be relieved and the pain score can be reduced by independently orally taking the composition only containing one of the antibodies; by taking the composition containing two or three IgY antibodies, the pain relieving effect can be synergistically enhanced, and the highest pain relieving rate can reach 100%.

The invention discloses a humanized structure-oriented chemokine receptor 2 mutant and application thereof. The humanized structure-oriented chemokine receptor 2 mutant is characterized in that an amino acid sequence is shown as SEQ ID NO. 2. The invention also discloses an application of the humanized structure-oriented chemokine receptor 2 mutant in preparation of drugs for treating cerebral hematoma. According to the humanized, high-activity and low-immunogenicity CCR2 mutant protein provided by the invention, the design is based on a human CCR2 wild type sequence (UniProt login number: P41597-1), a human CCR2 extracellular functional region framework is completely reserved, the introduction of redundant sequences is avoided, and then targeted mutation is carried out aiming at the binding activity, the protein conformation stability and the solubility of CCL2. Cerebral hematoma removal and neurological function repair can be accelerated, and absorption of rat cerebral hematoma is promoted. The cerebral hemorrhage prognosis can be effectively improved.

The application belongs to the field of biological medicine, and particularly relates to a leprosy early diagnosis biomarker, a detection reagent and application thereof. The application provides a leprosy early diagnosis biomarker, which is one or more of CCL2 / MCP-1, IL-8, JAKM, ATP, ND1, SERP, FLJ10489, LINC00659, LOC34487, LOC101928143, MIR22 and NCF1C, 12 genes. The application finds that the differentially expressed genes can be used as useful biomarkers, and provide a good basis for the development of a blood detection method for rapid diagnosis of leprosy.

This invention provides an engineered platelet and its application in the preparation of anti-injury drugs for liver transplantation. This engineered platelet utilizes the natural liver tropism of platelets; upon reaching the site of liver injury, PLT-aCCL2 is specifically activated under local microenvironment stimulation, releasing loaded small-sized antibody fragments or active ingredients. This effectively penetrates deep into the liver parenchyma, overcoming the problem of poor tissue penetration of large-molecule protein drugs. Through this targeted delivery strategy, aCCL2 can efficiently and specifically block the physiological function of the chemokine CCL2, inhibiting the infiltration of peripheral monocytes into the liver, thereby blocking the initiation and amplification of the inflammatory cascade. Ultimately, this strategy significantly inhibits T-cell-mediated adaptive immune responses and acute rejection, effectively reducing graft injury and prolonging graft survival.

The invention discloses application of montelukast in preparation of a medicine for preventing and treating hepatolenticular degeneration, and belongs to the technical field of biological medicines. According to the application disclosed by the invention, the montelukast is found to specifically block a cysteinyl leukotriene (CysLTs) receptor, cut off a CysLTs-mediated inflammation cascade reaction and remarkably inhibit the expression of chemotactic factors (such as CCL2) and subsequent pathological recruitment of macrophages, so that the liver is protected from secondary immune inflammation injury induced by copper toxicity. The discovery proves that montelukast can be used as a new anti-inflammatory and liver-protecting strategy without copper expelling dependence, can solve the problem of inflammatory injury which cannot be improved by the existing copper expelling medicine, and avoids possible side effects caused by powerful copper expelling. Besides, the montelukast is a marketed medicine (old medicine) which has been widely and clinically applied for many years, is clear in pharmacokinetics and high in safety, and has huge clinical transformation potential and application prospect as a medicine for preventing and treating hepatolenticular degeneration.

The invention provides a biomarker for predicting the oncolytic activity of an oncolytic virus and application of the biomarker, the biomarker comprises CCL2, and further comprises PODXL2 and / or CCDC190. In the invention, the oncolytic virus therapy sensitivity can be screened by detecting the expression mode of the biomarker, and the biochemical detection result is associated with the oncolytic virus sensitivity, so that the method is convenient and rapid, and can be used for rapidly and accurately screening patients with better oncolytic virus therapy response.

The preparation method comprises the following steps: taking 3, 3 ', 5, 5'-tetramethyl benzidine (TMB), polyoxyethylene polyoxypropylene ether (Pluronic F-127) and polydopamine as raw materials under a dark condition to prepare mesoporous polydopamine nano-microspheres, adding the mesoporous polydopamine nano-microspheres into the mesoporous polydopamine nano-microspheres, carrying out ultrasonic dispersion on the mesoporous polydopamine nano-microspheres, carrying out ultrasonic dispersion on the mesoporous polydopamine nano-microspheres, carrying out ultrasonic dispersion on the mesoporous polydopamine nano-microspheres, and carrying out ultrasonic dispersion on the mesoporous polydopamine nano-microspheres so as to obtain the mesoporous polydopamine nano-microspheres. Dispersing the nanoparticles into a buffer solution, and sequentially adding the fuzhangling and a CCL2 antibody to obtain the sequential targeting multifunctional nanoparticles loaded with the fuzhangling. According to the invention, the removal rate of the monkshood on the ocular surface is slowed down through a porous nanostructure, and active oxygen is removed to relieve oxidative stress while CCL2 and corneal epithelial cell mitochondria are sequentially targeted and inflammatory circulation participated by cytokines (IL-1beta, IL-6 and TNF-alpha), MMP9 and T cells is blocked.

The purpose of the present invention is to provide: a biomarker useful for rapid testing and / or early testing of progressive pulmonary fibrosis (PPF); a PPF testing method using the biomarker as an index; a PPF diagnostic agent containing a detection agent for the biomarker; a PPF diagnostic kit including the detection agent for the biomarker; and the like. This progressive pulmonary fibrosis testing method comprises a step for measuring the expression level of a gene product of at least one gene selected from the group consisting of HAMP, CXCL8, SPP1, RNASE1, CCL13, SELENOP, PLTP, CCL18, APOE, CTSB, CTSZ, HMOX1, F13A1, CD163, CHI3L1, PLA2G7, CHIT1, FABP5, CTSL, MMP9, APOC2, TREM2, CCL2, APOC1, LGMN, SLC40A1, FOLR2, MS4A6A, MARCKS, TMEM176B, DAB2, STAB1, GPNMB, CSTB, SDS, LIPA, and SGK1.