43 results about "Inflammatory pathways" patented technology

The present invention is concerned with new compounds, and particularly those having a fused bicyclic ring substituted with an amidine moiety. These compounds are each potent inhibitors of Factor D of the alternate pathway of complement, C1s of the classical pathway of complement, Factors Xa, XIIa, VIIa and thrombin of the coagulation pathway, plasmin in the fibrinolytic pathway, and kallikrein and high molecular weight kininogen in the inflammatory pathways. These proteases, which have serine in their active site, are called serine proteases and they are pivotal to most of the processes of inflammation and coagulation. In fact, these various systems are interactive with one another and it is difficult to activate one pathway without it influencing the others.

This document provides methods and materials related to regulating inflammatory pathways. For example, compositions and kits containing two or more of an anticholinesterase compound, a choline compound, and a carnitine compound and methods for using the compositions and kits described herein to support acetylcholine function to regulate one or more inflammatory pathways are provided.

Activation of 5-HT_2A receptors using agonists at surprisingly low concentrations was shown to potently inhibit TNF-α-induced inflammation in multiple cell types. Significantly, proinflammatory markers were also inhibited by the agonist, (R)-DOI, even many hours after treatment with TNF-α. With the exception of a few natural toxins, no current drugs or small molecule therapeutics demonstrate a comparable potency for any physiological effect. TNF-α and TNF-α receptor mediated inflammatory pathways have been strongly implicated in a number of diseases, including atherosclerosis, asthma, rheumatoid arthritis, psoriasis, type II diabetes, depression, schizophrenia, and Alzheimer's disease. Importantly, because (R)-DOI can significantly inhibit the effects of TNF-α many hours after the administration of TNF-α, potential therapies could be aimed not only at preventing inflammation, but also treating inflammatory injury that has already occurred or is ongoing.

The subject invention pertains to methods of identifying miRNAs that are differentially expressed in a lymphatic vessel cell under a proinflammatory stimulus. The invention also pertains to profiles of miRNAs that are differentially expressed in a lymphatic vessel cell under a proinflammatory stimulus and their use as biomarkers for diagnosis of inflammation mediated diseases. The current invention also provides therapeutic agents for the treatment of inflammation mediated lymphatic diseases wherein the therapeutic agents are capable of modulating the activity of the miRNAs differentially expressed in a lymphatic vessel cell under a proinflammatory stimulus.

The invention relates to the technical field of natural drugs, and particularly relates to a preparation method and application of a herba chloranthi serrati extract. The invention provides the application of the herba chloranthi serrati extract. A CCK8 cell proliferation detection experiment shows that the herba chloranthi serrati extract has no cytotoxicity effect on HepG2.2.15, has an obvious inhibiting effect on HBsAg and HBeAg antigen secretion, and shows a better anti-hepatitis B virus application prospect. The content of AST in HepG2.2.15 cell supernatant can be reduced, and a better anti-liver injury effect is shown. Huvec cell model transcriptome data analysis shows that the gene expression level of inflammatory pathways such as a TNF signal pathway and an IL-17 signal pathway can be effectively regulated, and a better liver inflammation regulating function is achieved.

The invention provides a method for regulating the polarization state of macrophages. The method comprises the step of activating cholinergic anti-inflammatory pathways of the macrophages by adoptingcholinergic anti-inflammatory pathway agonists and/or vagus nerve electrical stimulation signals. According to the method in the invention, the cholinergic anti-inflammatory pathway agonists are adopted to stimulate the macrophages in vitro; or the electrical stimulation signals are adopted to stimulate vagus nerves in vivo; therefore, the cholinergic anti-inflammatory pathways are activated; polarization of M1 type macrophages is inhibited; polarization of M2 type macrophages is promoted; a regulating effect on macrophage polarization types is achieved; and the method has the important significance in the aspects of specifically regulating the functions of the polarized macrophages and diseases caused by the polarized macrophages.

The invention discloses a ganoderma lucidum extract as well as a preparation method and application thereof. The preparation method comprises the steps of preparation of a ganoderma lucidum water extract and preparation of a ganoderma lucidum ethanol extract. The ganoderma lucidum extract comprises a ganoderma lucidum water extract and a ganoderma lucidum ethanol extract. The application refers to the application of the ganoderma lucidum extract in preparation of anti-gastric ulcer medicines and food. Pharmacological tests prove the effectiveness of the extract in anti-gastric ulcer, and reveal the anti-gastric ulcer action mechanism of the extract as follows: the extract inhibits NF-kB/NLRP3 of an inflammatory pathway by inhibiting NF-kB P65 nuclear migration, so proinflammatory factors of gastric mucosa tissues are down-regulated, the inflammatory response is inhibited, and the anti-gastric ulcer effect is realized.

Use of dietary fibre material extracted from grasses of the Poaceae family such as sugarcane, sweet sorghum and bamboo for the alleviation of chronic inflammation through improvement in intestinal flora and reduction of pro-inflammatory pathways.

A multifunctional system in which a nanostructure (size range of about 10-1000 nm) degrades on exposure to an infection and its associated inflammatory milieu. The degraded nanostructures release the encapsulated drug during the process of degradation, where the kinetics of drug release is determined by the severity of the infection and inflammation. This degradation is triggered by proteases secreted by the pathogen, host polymorphonuclear leucocytes and other host cells. The nanostructures are conjugated to anti-TLR (Toll-like receptor) ligands for targeting the corneal epithelium and blocking the inflammatory pathway.

Clostridium difficile infection is the leading cause of hospital acquired antibiotic-associated diarrhea in the US (Bartlett, in 2006). The increased prevalence of circulating C. difficile strains poses a significant health threat to US health care facilities. Strains expressing the toxin C. difficile Transferase (CDT), in addition to Toxins A and B (TcdA and TcdB), are more virulent and are associated with higher mortality rates (Bacci et al., 2011). We recently identified a protective role for eosinophils against C. difficile pathogenesis (Buonomo et al., 2016). We have also defined CDT's ability to increase host inflammation and suppress protective eosinophils through a TLR2 dependent mechanism (Cowardin et al., 2016). How CDT promotes virulence and eosinophil suppression via TLR2 is still under investigation. We employed a genome-wide microarray approach to reveal divergent transcriptional profiles between protected (TLR2−/−) and unprotected (WT) mice infected with either CDT expressing or CDT mutant strains of C. difficile. This work revealed novel host mediated TLR2-dependent inflammatory pathways to CDT. We provide an unbiased framework for understanding the host immune response to the binary toxin CDT produced by C. difficile and how TLR2 signaling enhances virulence.

Adrenergic receptor modulating compounds and methods of using the same are provided. Also provided are methods of treating a subject for a disease or condition associated with an adrenergic receptor including administering a therapeutically effective amount of the subject compound. Aspects of the disclosure include a method of modulating an inflammatory pathway in a cell, such as the production of TNF-alpha in the cell. The method can include contacting a cell with β1-selective adrenergic receptor modulating compound to selectively activate a cAMP pathway over a beta-arrestin pathway in the cell. Pharmaceutical compositions and kits which include the subject compounds are provided.