562 results about "Signalling pathways" patented technology

The invention belongs to the technical field of biological medicine, and particularly discloses application of kaempferol in preparation of a medicine for treating chronic obstructive pulmonary disease. The invention provides application of kaempferol in preparation of a medicine for treating chronic obstructive pulmonary disease. The invention provides a medicine for treating chronic obstructive pulmonary disease. The medicine comprises kaempferol or pharmaceutically acceptable salt thereof as an active ingredient. The invention aims to provide the application of kaempferol in preparation of the medicine for treating the chronic obstructive pulmonary disease, and the chronic obstructive pulmonary disease is treated by adjusting an AMPK signal channel, a Hippo signal channel, an MAPK signal channel and a PI3K-AKT signal channel.

The invention relates to the technical field of biological medicines, in particular to rapamycin-induced extracellular vesicles and application thereof in preparation of a medicine for promoting wound repair. The rapamycin-induced extracellular vesicles can enhance the migration and tube forming ability of endothelial cells, so that angiogenesis is promoted; meanwhile, the proliferation and migration capabilities of macrophages can be inhibited, and the proportion of M1 type macrophages in a wound is reduced, so that the inflammatory response mediated by the macrophages is relieved; and the composition shows extraordinary effects in the aspect of accelerating wound repair. The biological activity of the extracellular vesicles induced by the rapamycin depends on the activation of a PI3K / Akt signal channel.

Disclosed in the present invention is a novel substituted heterocyclic compound having VAV1 target degradation activity. Specifically disclosed is a compound serving as a VAV1 target degradation agent and having the structure of formula (I), or a pharmaceutically acceptable salt, solvate, hydrate, isotopic substituent or isomer of the compound. The compound can be used for preventing or treating diseases related to VAV1 targets or signaling pathways.

The invention belongs to the technical field of microorganisms and fermentation engineering, and particularly relates to application of bifidobacterium longum subsp. Infantis Y46 in the aspects of enhancing cell defense and repair and regulating metabolic homeostasis of a host. The strain is isolated from infant feces. Animal experiments prove that living cell thalli of the bifidobacterium longum subsp. Infantis Y46, which are obtained by culturing an MRS liquid culture medium added with L-cysteine hydrochloride (0.05%, v / v), can significantly enhance the oxidative stress resistance of an organism and reduce the level of active oxygen in the organism compared with a control bacterium bifidobacterium longum subsp. Infantis 15697. Transcriptomics analysis shows that the bifidobacterium longum subsp. Infantis Y46 can enhance self-protection of cells and improve physiological imbalance caused by external pressure by regulating related signal channels of an organism. The action mechanism is closely related to signaling pathways related to cell defense, metabolic homeostasis and barrier functions. The invention provides a new strain resource and an application scheme for developing functional food or medicinal preparations for enhancing the health defense function of a human body.

The invention relates to an application of an intervention SNRK-MTA1 signal channel axis in preparation of a non-small cell lung cancer targeted therapy drug. The nucleotide sequences of the mRNA of the SNRK gene and the mRNA of the MTA1 gene are respectively as shown in SEQ ID NO.1-2. The invention innovatively provides a strategy for treating the non-small cell lung cancer through double-target combined intervention. According to the strategy, SNRK gene expression is improved through exogenous gene overexpression plasmids, and meanwhile MTA1 gene expression is silenced through the siRNA technology. In a non-small cell lung cancer model, the strategy of combined application of the SNRK-OE plasmid and siMTA1 can specifically up-regulate the SNRK mRNA level and knock down the MTA1 mRNA level at the same time, and the combined strategy shows a better anti-tumor effect than single intervention, and can more effectively inhibit the growth and migration of tumor cells. Based on the discovery, the SNRK-MTA1 signal pathway axis can be developed into a novel therapeutic target for non-small cell lung cancer, and is used for designing a drug combination scheme or a composite targeted drug.

The invention relates to a cyclopeptide inhibitor aiming at human STING (stimulating interferon gene) and application of the cyclopeptide inhibitor. The cyclic peptide can specifically bind to and inhibit activation of human STING. The invention also provides a nanoparticle delivery system for loading the cyclopeptide on a cationic polymer PBAE and an amphiphilic polymer pDMA-pEPEMA, and a preparation method of the nanoparticle delivery system. The cyclic peptide and the nanoparticles thereof can be used for preparing medicines for treating autoimmune diseases (such as systemic lupus erythematosus and the like) caused by excessive activation of the cGAS-STING signal pathway. Compared with the existing small molecule STING inhibitor, the cyclopeptide inhibitor provided by the invention has higher specificity, stability and inhibition effect.

The invention discloses design and synthesis of a series of brain-targeted ginsenoside Rg1 derivatives and application of the brain-targeted ginsenoside Rg1 derivatives in treatment of Alzheimer's disease. According to the invention, ginsenoside Rg1 and polyethylene glycol with a specific chain length are covalently linked to successfully construct the derivative capable of enhancing the penetrating power of the blood-brain barrier. The series of derivatives provided by the invention not only solve the problems of poor brain targeting and insufficient stability of natural Rg1, but also can inhibit neuroinflammation by regulating and controlling an NLRP3 / caspase-1 signal channel in an LPS-induced neuroinflammation model, and finally, the learning and memory ability is remarkably improved. The product is simple and convenient in preparation process and good in biological safety, and a new candidate compound is provided for developing a new generation of Alzheimer disease treatment medicines.

Disclosed herein are small molecule compounds, compositions, formulations, and methods of modulating gpl30. Compounds, compositions, and formulations described herein are capable of modulating pro-inflammatory, fibrotic and / or regenerative responses. The disclosure also provides methods for treating or ameliorating disease, disorders and conditions associated with gp130 activity, particularly those associated with inflammatory and degenerative disorders, or combination thereof.

The invention provides application of G3BP1 in preparation of a medicine for protecting barrier function integrity of vascular endothelial cells, and belongs to the technical field of biological medicine manufacturing. The invention provides application of G3BP1 in preparation of a medicine for protecting barrier function integrity of vascular endothelial cells. The present invention relates to G3BP1 that ensures the sustained expression of key adherent junction proteins (VE-cadherin, p120) by directly binding to and stabilizing the mRNA of these proteins; meanwhile, the G3BP1 is combined with the MYD88mRNA to promote the degradation of the MYD88mRNA, so that a permeability-promoting MYD88-ARNO-ARF6 signal channel is inhibited, especially under the condition of an inflammation period. Therefore, the G3BP1 regulates and maintains the integrity of the vascular barrier through double transcription, and a new treatment strategy is provided for damage repair of the functional integrity of the vascular endothelial cell barrier.

The invention relates to a diatomic iron-iron site nano-enzyme constructed by relieving oxidative stress and cartilage degeneration and used for targeted osteoarthritis treatment. According to the invention, a nitrogen-doped porous carbon anchored diatomic iron nano enzyme catalyst (Fe2-NCs) with Fe-Fe dimer coordination is developed by using a'subject-object 'strategy. The Fe2-NCs protect cartilage cells from oxidative stress induced apoptosis by modulating ROS and active nitrogen species (RNS) and promoting O2 release. In addition, Fe2-NCs restores mitochondrial function by inhibiting NOX4 expression, improving ATP production, and normalizing COXIV levels. In an in-vivo OA model, the Fe2-NCs can reduce the expression of a pro-inflammatory medium COX-2 through an NF-kappa B signal channel, inhibit the up-regulation of MMP-13 and delay the degradation of type II collagen. The invention provides a new theoretical framework and methodological approach for the treatment of osteoarthritis, and has important clinical and scientific significance.

The invention provides a nerve growth factor functionalized exosome as well as a preparation method and application thereof. The functionalized exosome can activate a Wnt / beta-catenin signal channel to maintain dryness of corneal limbal stem cells (LSCs) so as to promote corneal epithelium repair, can activate a cAMP signal channel to relieve inflammatory response and promote corneal nerve regeneration, and can be used for treating or relieving corneal chemical burns, including relieving inflammatory response, reducing stromal scar formation and inhibiting corneal neovascularization. Corneal epithelium repair and nerve regeneration are promoted.

The invention discloses application of sodium butyrate in preparation of a medicine for relieving brain injury caused by gas explosion, the sodium butyrate regulates nerve cell ferroptosis through a JNK / P38 MAPK pathway to relieve the brain injury caused by gas explosion, firstly, an animal model of rat brain injury caused by gas explosion is established, and the relation between NaB and brain tissue neuron injury is intervened and observed by applying NaB; secondly, a shock wave physiotherapy instrument is used for impacting a co-culture system of three cells of CTX, H19-7 and GMI-R to simulate explosion to construct an in-vitro experimental model, P38, ERK and Fer-1 inhibitors are adopted for intervention, iron metabolism, ferroptosis and MAPK signal channel factor changes are observed from the cell and molecular level, a mechanism for inhibiting ferroptosis through a related cascade signal channel mediated by NaB-mediated intestinal-brain axis regulation and control is clarified, and the effect of inhibiting ferroptosis is achieved. And a theoretical basis is provided for further explaining the action mechanism of the gas explosion brain injury.

This document provides methods and materials involved in treating cancer. For example, methods and materials for modulating (e.g., increasing or decreasing) an interleukin-1 (IL-1) signaling pathway (e.g., an IL-1βsignaling pathway) during an adoptive cell therapy (e.g., a chimeric antigen receptor (CAR) T cell therapy) are provided. In some cases, one or more inhibitors of an interleukin-1 receptor antagonist (IL-1RA) polypeptide can be used to increasing IL-1 signaling (e.g., to reduce immunosuppression of the administered cells). In some cases, CAR T cells having a reduced level of an interleukin 1 receptor, type I (IL-1R1) polypeptide can have decreased IL-1 signaling (e.g., to reduce T cell toxicity associated with the administered cells).

The invention belongs to the field of biological medicines, and particularly discloses application of uridine in preparation of medicines for preventing and treating ulcerative colitis, including application of uridine in preparation of medicines for preventing and treating ulcerative colitis in acute stage, application of uridine in preparation of medicines for preventing and treating ulcerative colitis in remission stage and the like. Uridine can improve the symptoms of DSS-induced acute experimental colitis model mice, has a good treatment effect, and improves the weight of the model mice; experimental results indicate that a high-dose group of uridine has a good treatment effect, the mechanism and specificity of uridine up-regulate expression and activity of colon local SIRT1 protein, further inhibit phosphorylation activation of an NF-kappa B signal channel, regulate secretion of inflammatory factors and expression of tight junction protein, repair intestinal mucosal barrier while moderately regulating immunity, and improve the immunity of a human body. The systemic inflammatory response is effectively relieved.

The invention belongs to the technical field of biology, and particularly relates to an anti-hair-loss fish collagen peptide composition with a hair follicle signal channel regulating and controlling function and application of the anti-hair-loss fish collagen peptide composition. The composition can activate a Wnt / beta-catenin signal channel, inhibit a BMP channel, promote hair follicle growth period conversion and hair papilla cell proliferation, repair hair quality and improve the scalp microenvironment at the same time. The composition can be prepared into an oral preparation or an external scalp care product, has the advantages of safety, high efficiency and multi-target regulation, and is suitable for alopecia prevention and hair quality repair.

The present invention relates to a method for preparing organ-specific mesenchymal cells from pluripotent stem cell-derived intestinal organoid stromal cells. By using cells derived from stromal cell layers adjacent to intestinal organoids for differentiation into organ-specific mesenchymal cells, the present invention can greatly increase the efficiency of differentiation into stromal cells through the regulation of retinoic acid (RA) and hedgehog (HH) signaling pathways, and can increase the expression of organ-specific markers without exhibiting undifferentiated state cell characteristics, and thus mesenchymal cells having well-simulated biological characteristics can be prepared.

The invention relates to an application of a small molecule medicine STK000311 in a medicine for treating a cGAS-STING pathway abnormal activation disease, and belongs to the technical field of biological medicines. According to the application disclosed by the invention, the small-molecular medicine STK000311 or the pharmaceutically acceptable salt of the small-molecular medicine STK000311 serving as the cGAS-STING signaling pathway inhibitor has an obvious treatment effect on the cGAS-STING pathway abnormal activation diseases for the first time, and verification experiments show that the small-molecular medicine STK000311 can be used for obviously inhibiting the activity of human cGAS protein in a targeted manner and inhibiting cGAS-mediated antiviral immune response; the transcription level of ISGs in PBMCs (peripheral blood mononuclear cells) of an SLE (systemic lupus erythematosus) patient is inhibited, the fact that the small-molecule medicine STK000311 has huge potential of developing cGAS activity related diseases is fully proved, a novel treatment medicine is provided for clinic, and the small-molecule medicine STK000311 has good clinical application value and wide application prospect.

The invention discloses a heterocyclic aryl or heteroaryl-heteroaryl derivative and application of the heterocyclic aryl or heteroaryl-heteroaryl derivative. The heterocyclic aryl or heteroaryl-heteroaryl derivative of the present invention is a compound of formula (I), a stereoisomer thereof, an atropisomer thereof, a pharmaceutically acceptable salt thereof, a pharmaceutically acceptable salt of a stereoisomer thereof, a pharmaceutically acceptable salt of an isomer thereof, a solvate thereof or a pharmaceutically acceptable salt of a solvate thereof. The compound disclosed by the invention has good inhibitory activity on a 20-hydroxyeicosatetraenoic acid (20-HETE) signal channel, and has a good medicinal prospect. # imgabs0 #

Disclosed are in vitro methods for the differentiation of precursor cells into a neural crest cell (NCC) primed to a neurogenic lineage. The methods may include, for example, the steps of activating a Hedgehog signaling pathway (“HH signaling pathway”) in a precursor cell, wherein the precursor cell may be contacted with a neural crest cell induction medium for differentiation of the precursor cell into a neural crest cell. Compositions for carrying out the disclosed methods are also disclosed.

Disclosed is a composition and method for a therapeutic treatment that is able to combat triple negative breast cancers (TNBCs). The class of urea compounds acts by blocking at inhibiting the mTOR signaling pathway, which, as a central regulator of mammalian metabolism and physiology that when inhibited leads to the induction of autophagocytosis. The disclosed compounds are further capable of reinitiating the p53 cycle as well as inhibition of the BNIP3 / BNIP3L pathway. The disclosed compounds also shows the ability to cross the blood-brain-barrier where metastases can form. This new drug has the potential to be a powerful new treatment to combat invasive TNBCs.

The invention provides an application of protocatechuic acid in an anti-inflammatory active pharmaceutical composition in dairy cow mammary epithelial cells, belongs to the technical field of bioengineering, and aims to obtain high-purity protocatechuic acid (greater than or equal to 95%) by optimizing a preparation process through the application of protocatechuic acid in inhibition of inflammatory response of dairy cow mammary epithelial cells. Under the concentration of 1-100 mu M, the level of inflammatory factors such as TNF-alpha, IL-6 and the like is remarkably reduced (the inhibition rate is larger than or equal to 60%), the mechanism is that NF-kB and MAPK signal channels are inhibited, cytotoxicity is avoided, and a milk region perfusion agent or a feed additive can be prepared to be used for preventing and treating dairy cow mastitis.

The invention provides light-cured bio-ink, a digital light processing 3D printing product, a preparation method of the digital light processing 3D printing product and application of the digital light processing 3D printing product in preparation of a skull repair material, and belongs to the technical field of biological medicine. The material provided by the invention can continuously release HO under different environmental conditions. Particularly, in a simulated in-vivo environment, the GHDP hydrogel keeps stable HO release for a long time, so that a signal channel related to angiogenesis is continuously activated, and in the skull defect repair process, the GHDP hydrogel can promote neovascularization and osteogenic differentiation by regulating and controlling the HO level, so that the skull defect repair effect is improved. And a new strategy and thought are provided for promoting tissue regeneration by utilizing redox signal regulation and control.

The invention discloses application of (20S)-ginsenoside Rh1 in preparation of drugs for preventing and / or improving cerebral arterial thrombosis, and relates to the technical field of medical application of natural drugs. The invention verifies that (20S)-ginsenoside Rh1 up-regulates the expression of an anti-apoptosis gene by promoting STAT3 phosphorylation and translocation to a cell nucleus, so that the (20S)-ginsenoside Rh1 plays a role in protecting neuronal injury induced by sugar oxygen deprivation. In MCAO model mice, the (20S)-ginsenoside Rh1 obviously relieves the symptom of ischemic cerebral apoplexy and has positive influence on neurodegenerative events related to cerebral infarction, and the anti-apoptosis and neuroprotection effects are most prominent. Mechanism research shows that (20S)-ginsenoside Rh1 plays a therapeutic role in PC12 cell and MCAO model mice by activating a JAK2 / STAT3 signal channel.

The invention provides an application of gastrodin in preparation of a medicine for treating peripheral neuropathy. According to the application disclosed by the invention, gastrodin can inhibit neuroinflammation mediated by microglia by inhibiting activation of an NF-kB / NLRP3 inflammasome signal channel, so that release of inflammatory factors is reduced, and neuropathy induced by bortezomib is relieved.

The present disclosure relates to the technical field of biomedicine, in particular to use of an interleukin (IL)-17A inhibitor in the preparation of a medicament for treating an inflammatory disease. Use of an IL-17A inhibitor in the preparation of a medicament for treating an inflammatory disease is provided. Studies have proved that tangeretin (Tan) shows a significant anti-inflammatory activity both in vivo and in vitro, and may reduce inflammatory responses by inhibiting production of pro-inflammatory factors (such as tumor necrosis factor (TNF)-α and IL-6) and regulating IL-23 / STAT3 / IL-17A signaling pathways. Moreover, as a natural medicament, Tan may more safely and stably inhibit production of IL-17A and thus serves as a desirable IL-17A inhibitor.

The present invention relates to methods and uses of CGRP signaling pathway activators for promoting antibody generation and vaccine protection, and related pharmaceutical compositions and vaccine compositions.

The invention discloses an anti-inflammatory CAR-macrophage targeting FAP, a preparation method thereof and application of the anti-inflammatory CAR-macrophage in preparation of drugs for treating fibrosis diseases, and belongs to the technical field of biological medicines. The invention provides an FAP-specific chimeric antigen receptor, an mRNA expression vector of the FAP-specific chimeric antigen receptor, a His-labeled STING signal channel inhibitor and an mRNA expression vector of the His-labeled STING signal channel inhibitor. In-vivo and in-vitro macrophage editing can be effectively realized by delivering CAR mRNA and TRIM13mNRA through LNP, the ability of targeted phagocytosis of FAP positive cells is endowed, meanwhile, anti-inflammatory phenotypic polarization of macrophages is promoted, local inflammation is improved, and fibrosis progress driven by inflammation is synergistically restrained.

The invention belongs to the technical field of biological medicine and molecular biology, and provides application of GJB6 in preparation of an esophageal squamous cell carcinoma prognosis evaluation reagent and screening of drugs for targeted treatment of esophageal squamous cell carcinoma. The low expression of the GJB6 is applied to preparation of an esophageal squamous cell carcinoma prognosis evaluation reagent. GJB6 is low in expression in ESCC patients, and ESCC prognosis is poor. And the prognosis of patients with high expression of GJB6 is better. Overexpression of GJB6 inhibits ESCC cell proliferation, migration and invasion and in-vivo tumor enlargement. The GJB6 plays a role of a cancer suppressor gene in ESCC and inhibits cell proliferation, migration and invasion. The AKT signal channel is one of downstream channels for GJB6 to regulate the occurrence and development of ESCC. The AKT inhibitor effectively inhibits GJB6 low-expression ESCC malignant phenotypes, including enhancement of cell proliferation and migration invasion ability and in-vivo tumor enlargement. The AKT is a key therapeutic target of the GJB6 low expression type ESCC.

This invention belongs to the field of pharmaceutical technology, specifically relating to a quinazoline-azaindole compound, its preparation method, and its application in treating Alzheimer's disease. The quinazoline-azaindole compound of this invention regulates NF-κB by inhibiting DYRK1A. k B. A series of signaling pathways, including PI3k-Akt, achieve anti-neuroinflammatory effects; quinazoline-azaindole compounds can reduce the expression of inflammatory factor-related genes in an LPS-induced BV2 microglial inflammation model, thereby reducing the levels of inflammatory factors in the hippocampus and cortex, alleviating neuronal pathological damage caused by neuroinflammation, and improving cognitive impairment caused by neuroinflammation; in summary, quinazoline compounds inhibit DYRK1A and downregulate NF-κB signaling pathways. k It can reduce the expression and release of inflammatory factors, improve brain tissue pathology, and alleviate cognitive impairment through signaling pathways such as B, and has significant clinical application value.

The invention belongs to the technical field of medicine, and particularly relates to an NLRP3 inhibitor, a preparation method thereof and application of the NLRP3 inhibitor in medicine. The invention provides an NLRP3 inhibitor as shown in a formula (I) as well as a composition and application thereof. The NLRP3 inhibitor can be used for treating or preventing diseases or symptoms related to abnormal expression of an NLRP3 signal channel. # imgabs0 #