142 results about "Lung Inflammations" patented technology

Disclosed is the use of an antagonist of Interleukin 1 receptor type 1 (IL-1R1) for the manufacture of a medicament treating, preventing or suppressing lung inflammation or a respiratory disease. In some embodiments of the described invention, the medicament is for local administration to pulmonary tissue. Also disclosed are methods for treating lung inflammation or a respiratory disease.

Described herein are methods and compositions for treatment of inflammation, such as inflammation in lung and/or airway tissue, including asthma Innate lymphoid cells (ILCs), such as type 2 ILC2s, are herein described as capable of IL-33 signaling activation, leading to airway hyperresponsiveness (AHR) and inflammation. Further described is the hereto unknown discovery that ICOS-ligand is expressed in ILC2s, that ICOS binding of ICOS to ICOS-ligand is required for its function in ILC2s, and that while IL-33 treatment induces AHR in control mice, IL-33 cannot induce AHR in mice receiving treatment via anti-ICOS-ligand antibodies. These results suggest new methods and compositions targeting ICOS and ICOS-ligand, such as dual specific antibodies that recognize ICOS and ICOS-ligand, an expression profile unique to ILC2s.

Methods of treating, reducing, or preventing lung infections or lung inflammation include identifying a patient in need of treatment and administering a therapeutically effective amount of at least one cationic steroid antimicrobial (CSA), or a pharmaceutically acceptable salt thereof. Treatment of cystic fibrosis lung infections, COPD lung infections, inflammation of the lungs in these patient populations, and lung scarring in these patient populations is also described.

The present invention relates to pharmaceutical kits and methods to treat lung inflammation and redox imbalance in human cystic fibrosis patients using pharmaceutical compositions containing N-acetylcysteine (NAC), pharmaceutically acceptable salts of N-acetylcysteine, or N-acetylcysteine derivatives. In phase I studies, treatment with oral NAC at a dose of from about 1800 mg/day to about 3000 mg/day for a period of 4 weeks produced significant positive effects, namely, it decreased absolute numbers of white blood cells and neutrophils in the sputum and produced concomitant decreases in sputum neutrophil elastase specific activity and sputum interleukin-8 levels, suggesting an amelioration of lung inflammation in the patients. These effects were associated with an increased total GSH level in whole blood as well increased staining for reduced GSH in blood neutrophils, both of which reflect an amelioration of the redox imbalance in the patients. In ongoing phase II studies, oral NAC at a dose of about 2700 mg/day administered in double-blind manner for 12 weeks showed excellent safety and significantly decreased white blood cells in sputum as compared to placebo.

The invention discloses Lactobacillus reuteri capable of relieving atopic asthma Th2 reaction and application of Lactobacillus reuteri and belongs to the technical fields of microorganisms and medicine. The Lactobacillus reuteri has an atopic asthma relieving function, specifically reflected as follows: (1) significantly reducing lung inflammation reaction of atopic asthma mice; (2) remarkably inhibiting production of total immunoglobulin IgE in serum of the atopic asthma mice; (3) significantly decreasing the content of IL-5 in lungs of atopic asthma mice; (4) significantly decreasing the content of IL-13 in lungs of atopic asthma mice; and (5) significantly raising the content of propionic acid in intestines of atopic asthma mice. Therefore, the Lactobacillus reuteri has great application prospects in preparation of a product for preventing and/or treating atopic asthma.

This invention relates to a sealed container containing a powder formulation comprising a dehydroepiandrosterone, its analogue(s) or salt(s) by itself or with a pharmaceutically or veterinarily acceptable carrier or diluent, and having a particle size of about 0.1 μm to about 100 μm. The formulation can be used to treat or prevent asthma, chronic obstructive pulmonary disease, lung inflammation, and other respiratory diseases or conditions. The formulation may be prepared by jet milling, and may be delivered through the respiratory tract or other routes using a nebulizer. The sealed container is provided in a device and/or a therapeutic kit.

Compositions and methods for the treatment of inflammation are provided.

The invention relates to compounds of formula (I):

or a pharmaceutically acceptable salt thereof, including all stereoisomers, tautomers and isotopic derivatives thereof, which are inhibitors of p38 mitogen-activated protein kinase enzymes (referred to herein as p38 MAP kinase inhibitors), particularly the alpha and gamma kinase sub-types thereof, and their use in therapy, including in pharmaceutical combinations, especially in the treatment of inflammatory diseases, including inflammatory diseases of the lung, such as COPD.

The invention relates to health protection tea and a preparation method thereof, in particular to health protection tea for treating chronic bronchitis and a preparation method thereof. The incidence rate of chronic bronchitis in middle-aged and old-aged populations is high, and chronic bronchitis is a common respiratory disease. In recent years, along with the aggravation of environmental pollution and the declination of air quality, people with chronic bronchitis have the development tendency of young change. The health protection tea for treating chronic bronchitis is guided by the theories of traditional Chinese medicine by combining with the tea drinking culture of China and is prepared from the raw materials of honeysuckle, apricot kernels, dried pineapple, loquat leaves, walnut kernels, licorice roots, Chinese mugwort leaves, ginger slices, red dates, dwarf lilyturf tuber, lily, dandelion, peppermint, cape jasmine, rhizoma anemarrhenae, fritillaria, tea leaves and honey through refining. The health protection tea can effectively eliminate lung inflammation, promote blood circulation, dissipate stasis, relieve a cough, disperse the lungs, promote the secretion of saliva and regulate qi, has outstanding curative effects on chronic bronchitis and can be dunk for a long time without any adverse drug resistance reaction and side effect.

The invention discloses lactobacillus reuteri capable of alleviating allergic asthma and application thereof and belongs to the technical field of medicines. The lactobacillus reuteri has an effect ofrelieving allergic asthma, which is embodied by: (1) significantly reducing lung inflammation in mice with allergic asthma; (2) significantly inhibiting the generation of dust mite specific immunoglobulin IgG1 in serum of allergic asthma mice; (3) significantly reduced the contents of IL-5 and IL-13 in alveolar lavage fluid of mice with allergic asthma; (4) significantly reducing the content of IL-17A in alveolar lavage fluid of mice with allergic asthma, and thus the lactobacillus reuteri has great application prospects in the preparation of products for preventing and/or treating allergic asthma.

This invention provides novel peptides and methods to prevent, control, and treat an inflammation, cancer and other disorders, particularly of the gastrointestinal tract and the lung by administering at least one agonist of guanalyte cyclase receptor either alone or in combination with a compound selected from i) 5-aminosalicyclic acid (5-ASA) or a derivative or a pharmaceutically acceptable salt thereof; ii) mercaptopurine; or iii) an anti-TNF therapy.

The invention relates to rehmanniae radix oligosaccharides, the method for preparing the same, and its application. The method comprises taking rehmanniae radix medicinal materials as raw material, extracting with and getting rehmanniae radix total sugar, separating with silica gel column and getting the oligosaccharides, mainly comprising stachyose, and. The content is more than 60%. It is demonstrated by pharmacodynamics experiment that the oligosaccharides can inhibit rat lung inflammation induced by lipopolysaccharide of coli bacillus, and can be used to prepare drug treating chronic obstructive pulmonary disease.

The invention relates to application of dendrobium officinale polysaccharides in preparation of harm-reducing cigarettes. Harm reduction means reducing risks of lung inflammation caused by smoking. The harm-reducing cigarettes are prepared by dissolving the dendrobium officinale polysaccharides by utilizing water, evenly spraying the dendrobium officinale polysaccharides on cut tobaccos, naturally airing the cut tobaccos, and then rolling the cigarettes according to regular cigarette rolling technology. The application of dendrobium officinale polysaccharides in preparation of harm-reducing cigarettes can reduce the occurrence rate of lung inflammation caused by smoking and reduce expression of kinase beta (IKKbeta) of a lung tissue nuclear factor Kappa B(NF-kB) inhibitor caused by smoking.

The invention discloses application of ginkgo biflavonoids to preparation of a medicine for preventing and treating asthma. The ginkgo biflavonoids are at least one of 7-demethylated biflavones, ginkgetin, sciadopitysin, and isoginkgetin. The invention discloses a medicinal composition for preventing and treating the asthma, the composition comprises ginkgo biflavonoids, and further comprises at least one of radix glycyrrhizae, white mulberry root-bark and semen armeniacae amarum. The invention further discloses a pharmaceutical composition formed by mixing ginkgo biflavonoids and a pharmaceutically acceptable excipient, and the mass percent of ginkgo biflavonoids is greater than and equal to 2.5%. The ginkgo biflavonoids can inhibit the recruitment of inflammatory cells in lungs, reduce the expression of inflammatory factors in the lungs, and lower the expression of PI3K-related proteins in inflammation pathways, and are free of obvious toxic or side effects and safe and reliable after being taken for a long term.

This invention provides compounds of Formulae (IA), (IB), (IC), (ID), (IE), (IF), (IG), (IH), (IJ), (IK), (IL), (II), (III), (IIIA), and (IIIB); pharmaceutically acceptable salts and solvates thereof; and compositions thereof. This invention further provides methods for treating a disease, including but not limited to, liver disease or an abnormal liver condition; cancer (such as hepatocellular carcinoma or cholangiocarcinoma); a malignant or benign tumor of the lung, liver, gall bladder, bile duct or digestive tract; an intra- or extra-hepatic bile duct disease; a disorder of lipoprotein; a lipid-and-metabolic disorder; cirrhosis; fibrosis; a disorder of glucose metabolism; a cardiovascular or related vascular disorder; a disease resulting from steatosis, fibrosis, or cirrhosis; a disease associated with increased inflammation (such as hepatic inflammation or pulmonary inflammation); hepatocyte ballooning; a peroxisome proliferator activated receptor-associated disorder; an ATP citrate lyase disorder; an acetyl-coenzyme A carboxylase disorder; obesity; pancreatitis; or renal disease.

The present invention discloses a use of cholesterol-modified HuR interference siRNA in preparation of drugs for treating acute lung injury caused by sepsis. According to the present invention, the related HuR interference siRNA is an artificially-synthesized and cholesterol-modified small nucleic acid drug; with intravenous administration, results show that the HuR siRNA can be richly distributed in lung tissue, enter lung cells, inhibit a plurality of 3'-UTR of mRNA of inflammatory factors having HuR binding sites, and promote TNFalpha RNA degradation so as to inhibit acute lung injury induced by bacterial lipopolysaccharide (LPS), wherein TNFalpha expression can be inhibited; and the small nucleic acid drug provides significant release effects for lung inflammation, is applicable for intravenous administration, inhalation administration or intratracheal administration, and is the small nucleic acid drug having application values and prospects and provided for treating acute lung injury under the premise of lack of effective and related acute lung injury treatment nucleic acid drugs in the prior art.