31 results about "Macrophage infiltration" patented technology

This invention relates to methods and compositions for the treatment and diagnosis of cardiac diseases and disorders, such as cardiac hypertrophy, myocardial infarction, stroke, arteriosclerosis and heart failure. The invention also relates to methods and compositions for the treatment of fibrosis-related diseases as well as methods and compositions for reducing apoptosis, increasing ST2L signaling, decreasing NF-κB activation, decreasing IκBα phosphorylation, decreasing P38MAPK phosphorylation, decreasing JNK phosphorylation, decreasing reactive oxygen species generation, decreasing macrophage infiltration and/or decreasing the expression of hypertrophic genes. More specifically, the invention relates to IL-33 and/or soluble ST2 inhibiting agents for use in the methods and compositions provided.

The invention relates to methods and compositions for the treatment or prevention of ocular angiogenesis and neovascularization associated with neovascular disease. Administration of vascular endothelial growth factor (VEGF)-A into the eye when macrophage infiltration is reduced inhibits ocular angiogenesis.

The invention relates to the design and synthesis of 3-arylidene-anabaseine compounds that exhibit enhanced selectivity toward alpha7 nicotinic receptors. The compounds are expected to be useful in treating a wide variety of conditions, including neurodegenerative conditions such as Alzheimer's Disease, neurodevelopmental diseases such as schizophrenia, and certain peripherally located inflammations mediated by macrophage infiltration.

The invention provides an application of flavonoids compounds in the preparation of a T lymphocyte subsets regulating drug. The innovative discovery of the invention is that the flavonoids compounds can regulate the proportion of T lymphocyte subsets, so that the effect of immune system is regulated, and the related pathological injury can be cured. Specifically, the proportion of a CD4+IFN-gamma+Th1 cell subset, a CD4+IL-17+Th17 cell subset and a CD4+CD3e+CD62L+ThO cell subset can be lowered, and the proportion of CD4+CD25+Fo8*p3+Treg cell subset is increased. Chrysin can maintain the integrity of the blood-retinal barrier of an EAU mouse, inhibit the macrophage infiltration, and inhibit the intraocular inflammation. At the same time, the expression quantity of retinas STAT1, STAT3 and phosphorylated protein is inhibited. Based on new properties of the flavonoids, the flavonoids can be applied for curing a plurality of diseases with the effect of proportional imbalance of T cell subsets.

Methods of inhibiting inflammation and macrophage infiltration following spinal cord injury and methods of modulating the release of TNF-α from cells expressing α-d are disclosed. Anti-α-d monoclonal antibody was used to block the binding between α-d and VCAM-1. A hybridoma secreting the antibody and a diagnostic method using the antibody are disclosed.

The invention relates to a method for constructing a kidney persistent innate macrophage infiltration rat model. The method includes the step of specifically expressing an IL34 gene in a rat kidney tubules cell. Preferentially, a totipotential cell contains a Cre recombinase expression frame and an IL34 condition expression frame driven by a kidney tubules tissue specific promoter at the same time, and the IL34 condition expression frame comprises a target gene expression promoter, a transcription barrier segment with loxp sequences in the same direction at the two ends, and an IL34 gene coding frame. The method has the advantages that by constructing a kidney tubules height expression IL34 rat, the kidney rat model with innate macrophages as the main infiltration characteristic is successfully constructed, unselective gene over-expression and unselective cell infiltration can be effectively avoided, the influences on the overall state of important organs outside a kidney and an organism are reduced, and the specificity of the kidney innate macrophage infiltration can be effectively improved.

ACE receptors are affected in severe acute respiratory distress syndrome related coronaviruses. ACE genes are directly related to the morbidity and mortality of those with cystic fibrosis. The thick, sticky mucus in the respiratory, and digestive systems, is seen in the inherited disease cystic fibrosis. Viral induced sticky mucus in the respiratory and digestive systems can also be appreciated as a response to viral pathogens where the cycle of mucus production in vivo induces the recruitment of more mucus production to the extent that cellular damage occurs within the lower respiratory track requiring intubation as a life saving measure. In the most severe cases mechanical intubation fails due to the fact that no control over the recruitment of mucus production was achieved at the onset. SARS pathology shows inflammatory exudation in the alveoli and interstitial tissue, with hyperplasia of fibrous tissue and fibrosis. Inherited cystic fibrosis pathology shows atelectasis, mucoid impaction, acute and chronic inflammation, bronchiectasis, cyst formation, and fibrosis widespread. A virally induced disorder in relations to ACE2 receptors can be treated successfully at the early onset with inherited cystic fibrosis disease mimicking techniques with the efforts of minimizing the activity and utilization of the ACE2 receptor. Cystic fibrosis lung infections, and opportunistic pathogens contribute to chronic airway inflammation that is characterized by neutrophil/macrophage infiltration, cytokine release and ceramide accumulation. In terms of virally induced forms off ACE2 receptor pathologies, as it related to coronavirus such as Covid 19, presumably ceramide precursors which aid in intracellular transport of the virus into the cell via inflammation and remodeling is present in alveolar tissues of the lung in patients with cystic fibrosis while the same pathology occurs in patients with virally induced forms of ACE2 pathology which to often progresses to SARS or ARDS.

The invention belongs to the technical field of medicines, and discloses application of IELLQAR as medicine for preventing and treating atherosclerosis diseases. The IELLQAR can inhibit the binding ofmononuclear cells and P, E and L selection glycoprotein so as to inhibit the adhesion of mononuclear cells and endothelial cells, and also has a function of inhibiting inflammation. An ApoE gene mouse is induced by high fat diet, then obvious atherosclerosis plaques can be seen in the aorta, IELLQAR intervention can retard ApoE gene knockout mouse atherosclerosis lesions, and local mononuclear macrophage infiltration of atherosclerosis plaques can be reduced. Animal experiments and in vitro cell research levels indicate that the IELLQAR can inhibit mononuclear cell adhesion and inflammatory factor expression, atherosclerosis progress can be inhibited through an anti-inflammatory mechanism, atherosclerosis-related diseases can be prevented and treated, and therefore, the IELLQAR has an important clinical application prospect.

The present invention relates to the discovery that non-traditional export of certain pro-inflammatory cytokines lacking a signal sequence from a cell can be inhibited by copper chelation and/or administration to the cell of a truncated form of S100A13 lacking the basic residue portion. Further, copper chelation inhibits, inter alia, neointima formation, macrophage infiltration and associated inflammation, cell proliferation, secretion of extracellular matrix, intimal thickening, adventitial angiogenesis, restenosis, and the like, associated with vascular vessel injury. Thus, the present invention provides novel methods of preventing and treating, and for identifying novel compounds also useful as therapeutics for, such conditions.

The invention discloses a medicinal composition for preventing and treating atherosclerosis. The medicinal composition comprises tanshinone II-A and atorvastatin, wherein the weight part ratio of the tanshinone II-A to the atorvastatin is preferably 10:(2-10); the tanshinone II-A is combined with the atorvastatin as a statin drug for use, so that the curative effect of high dosage of the tanshinone II-A or the atorvastatin can be achieved by a small dosage of the combined tanshinone II-A and atorvastatin, and the synergistic effect is obvious after drug combination; thus the areas of a lipid core and plaques can be obviously reduced, macrophage infiltration is reduced, collagen content in the plaques is increased, conditions of activation of NF-kB (Nuclear Factor-kappa B) are reduced, production of active oxygen in arterial plaques is inhibited, and the like. The medicinal composition for preventing and treating atherosclerosis has broad application prospect.

Provided herein are peptide-based hydrogels, or neutral multidomain peptide hydrogel (NMDP), as well as uses thereof. The uses include encapsulating cells to induce quiescence for long-term storage and administering to a subject to induce collagen deposition and macrophage infiltration. The disclosed hydrogel is useful for the preservation of stem cells, including maintaining their quiescence and differentiation potential.

An antibody, preferably a blocking antibody, and most preferably a monoclonal antibody (mAb), specific for human endothelial cell protein C receptor (EPCR) such as mAbs JRK 1494 or JRK 1535 is used to reduce or attenuate joint swelling, macrophage infiltration, iron deposition and/or blood vessel formation and to treat arthropathy in a hemophilic subject.

The invention provides an anti-allergic composition and an application of the anti-allergic composition in preparation of an anti-allergic preparation. The traditional Chinese medicine effective components and the composition thereof comprise amygdalin, cimicifugin, a composition of the amygdalin and the cimicifugin, a composition of the amygdalin and the 5-O-methylvisammioside, and a composition of the cimicifugin and the 5-O-methylvisammioside, which have obvious interaction with macrophage migration inhibition factors. The migration quantity of zebrafish macrophages can be obviously inhibited; the application of the anti-allergic composition in the preparation of the anti-allergic preparation is characterized in that the anti-allergic pharmaceutical composition can be used for treating allergy-related diseases caused by macrophage infiltration, migration and inflammatory factor release caused by allergy, including allergic rhinitis, allergic asthma, allergic rash and allergic purpura, as well as allergic rhinitis, allergic asthma, allergic rash and allergic purpura. And important drug guidance is provided for treatment of allergic diseases.

The invention discloses application of DHC (dehydrocorydaline) in preparation of a preparation for treating atherosclerosis. ApoE<-/->mice prove that formation of atherosclerotic plaques treated by the DHC is reduced, the lesion area of the plaques is reduced, and it is indicated that DHC can relieve development of atherosclerosis. An oil red O staining result shows that the grease area of an administration group is reduced, F4/80 immunofluorescence staining shows that macrophage infiltration of the administration group is less, and a Masson staining result shows that the fiber collagen content of the administration group is higher, which indicates that the DHC can improve the stability of plaques. Administration of the DHC can also reduce systemic inflammation of atherosclerosis. An important scientific evidence is provided for potential application of the DHC as an atherosclerosis treatment or improvement agent.

The invention provides application of an inhibitor of histone methyltransferase DOT1L in preparation of a medicine for preventing and treating peritoneal fibrosis after peritoneal dialysis. EPZ5676 isused for inhibiting histone lysine methyltransferase DOT1L, so that the peritoneal pathological change caused by high-glucose peritoneal dialysis fluid damage can be relieved, and the peritoneal function is improved. The inhibition mechanism is mainly characterized in that the EPZ5676 inhibits peritoneal mesothelial cell-mesenchymal transdifferentiation, and reduces inflammatory cell infiltration, especially macrophage infiltration. Therefore, DOT1L can become an important target spot for preventing or treating peritoneal fibrosis, and the related inhibitor is expected to become a clinical medicine and is used for preventing or treating peritoneal fibrosis related to peritoneal dialysis.

Methods to inhibit inflammation and macrophage infiltration following spinal cord injury are disclosed along with methods to modulate TNFα release from cells expressing α_d are disclosed.