16 results about "ABCA1" patented technology

One aspect of the present invention relates to: a conjugate comprising a peptide of a novel sequence and glycyrrhizin; and a pharmaceutical composition for preventing or treating obesity, the composition comprising the conjugate. The conjugate and composition comprising same according to one aspect were found to inhibit hypertrophy of fat cells, increase the cell membrane expression level of ATP-binding cassette transporter A1 (ABCA1), and reduce the secretion of tumor necrosis factor-α (TNF-α). In addition, the conjugate and composition comprising same were found to remain in a greater amount in the blood and have better pharmacokinetic properties than glycyrrhizin used by itself, and thus can be used in the obesity prevention and / or treatment market / industry.

The invention provides an oil control composition as well as a preparation method and application thereof. The oil control composition is prepared from the following components in parts by weight: 20 to 60 parts of rhizoma anemarrhenae root extract, 2 to 20 parts of swertia bimaculata extract and 10 to 90 parts of solvent. Experiments show that the oil control composition can play a role in inhibiting expression of regulatory factors SREBP-1, SCD1 and FASN, meanwhile, expression of AMPK is promoted, and generation of grease is effectively inhibited by precisely regulating and controlling the targets; on the other hand, the oil control composition can also promote expression of ABCA1 and accelerate discharge of generated grease, so that the comprehensive oil control effect is achieved.

The invention belongs to the technical field of insecticides, and particularly relates to a ds-ABC transporter gene for preventing and controlling resistant Frankliniella occidentalis as well as a screening method and application of the ds-ABC transporter gene. The ABC transport protein gene is selected from any one or more of ABCG20, ABCA1, ABCB8, ABCD2 and ABCA5, and the ABC transport protein gene is selected from any one or more of ABCG20, ABCA1, ABCB8, ABCD2 and ABCA5. The screening method comprises the following steps: (1) testing the resistance level of the Frankliniella occidentalis to spinetoram, imidacloprid and thiamethoxam; (2) extracting and purifying the total RNA of the Frankliniella occidentalis population by using a trace total RNA extraction kit, synthesizing cDNA (complementary deoxyribonucleic acid) by taking the RNA as a template, and then carrying out quantitative primer design and gene expression; and (3) carrying out significant analysis on difference analysis of all data through real-time fluorescent quantitative detection, and screening out 5 ds-ABC transporter genes which are subjected to significant up-regulation expression in a resistant population. According to the invention, the key ABC transporter gene for mediating the resistance of the Frankliniella occidentalis to the spinetoram is screened and determined, and a basis is provided for development of a novel anti-resistance insecticide taking the ABC transporter as a target.

The invention relates to the technical field of biological medicine, and particularly discloses a lipidosome targeting SELENOP + macrophages, a preparation method of the lipidosome and application of the lipidosome in lung squamous cell carcinoma treatment. According to the lipidosome, an SELENOP antibody is used as a targeted modification molecule, si-SELENOP and s-ABCA1 / G1 are loaded, and accurate delivery of siRNA in target cells is achieved through specific binding of the antibody and a SELENOP receptor on the surface of a SELENOP + macrophage. The targeting liposome prepared by the invention can specifically inhibit cholesterol efflux pathways of SELENOP + macrophages, reverse tumor phenotypic polarization, remodel a tumor immune microenvironment and recover anti-tumor activity of immune cells such as CD8 + T cells, NK cells and the like. When the liposome is independently used or combined with a PD-1 antibody, the growth and metastasis of the lung squamous cell carcinoma can be remarkably inhibited, the treatment effect is improved, a brand new metabolism-immunity synergistic targeted treatment strategy is provided for the lung squamous cell carcinoma, and the liposome has a good clinical application prospect.

The invention belongs to the technical field of dermatan sulfate application, and particularly relates to application of dermatan sulfate in promotion of cholesterol excretion. The cholesterol excretion promoting effect of dermatan sulfate is discussed through in-vivo and in-vitro experiments, and results show that dermatan sulfate has the effect of promoting cholesterol excretion of liver cells, not only can reduce blood fat and liver lipid and promote excretion of cholesterol to excrement, but also can inhibit expression of ASGR1, further up-regulates LXR alpha, and has the effect of promoting cholesterol excretion of liver cells. The expression of ABCA1 and ABCG5 transporters is improved to promote cholesterol excretion and reduce the in-vivo lipid level. Therefore, dermatan sulfate is a potential medicine for promoting cholesterol excretion, a new thought is provided for development of a targeted ASGR1 medicine for promoting cholesterol excretion, and a theoretical basis is provided for treatment of cardiovascular diseases such as hypercholesterolemia and the like.

The present application relates to the technical field of biological medicine, and in particular to a reagent for regulating an ALKBH5-ABCA1 axis and application of the reagent in preparation of a drug for treating glaucoma, wherein the reagent at least includes any one of a reagent for promoting expression of ALKBH5, a reagent for promoting expression of ABCA1, a reagent for inhibiting expression of METTL3, and a DNA methyltransferase inhibitor for a promoter region of ALKBH5 gene.The present application provides a reagent for targeting activation of ABCA1 or a reagent for specifically targeting delivery of ALKBH5 mRNA to a trabecular meshwork, and the reagents can effectively reverse lipid metabolism defects and significantly reduce intraocular pressure.The present application not only provides a novel treatment target based on epigenetics and metabolism for glaucoma, but also realizes a proof of concept of LNP-mRNA intraocular pressure reduction technology for the first time, and has a very high clinical conversion value.

The present invention provides a novel use of 25-hydroxycholesterol (25HC), a natural metabolite in vivo, for treating rifampicin (RFP)-induced hepatic lipid deposition. 25HC is a metabolite of cholesterol produced by cholesterol 25-hydroxylase (CH25H). Previously, it has been reported to exhibit antiviral, interferon-activating, anti-tumor, and lipid metabolism activities. The present invention finds that RFP can induce hepatic steatosis, lipid droplet deposition, and reduce CH25H expression. Therefore, 25HC deficiency may be one of the mechanisms by which RFP induces hepatic lipid deposition. The present invention is the first to discover that 25HC supplementation can alleviate RFP-induced lipid droplet deposition (reduction in both triglycerides and cholesterol). In particular, it is the first to discover that the mechanism by which 25HC reduces liver cholesterol content is related to promoting LXRα expression and entry into cells, and promoting the expression of cholesterol efflux genes ABCA1, 2, and 3. This suggests that 25HC may reduce liver lipid deposition and alleviate RFP-induced liver damage by promoting cholesterol efflux from hepatocytes, laying the foundation for the future clinical application of 25HC.

The invention discloses an application of ABCA1 as a steady-state regulation target of lung cholesterol. By constructing a CYP27A1 gene knockout mouse model and combining molecular biology and RNA (Ribonucleic Acid) sequencing technologies, the invention further discloses a potential relationship between down-regulation of ABCA1 in liver tissues and specific up-regulation of ABCA1 in lung tissues and cholesterol. The research of the invention not only helps to deepen the understanding of the role of the ABCA1 in the lung cholesterol homeostasis, but also provides theoretical support for the prevention and treatment of cholesterol metabolism related diseases, and defines that the ABCA1 can be used as a target spot for regulating and controlling the lung cholesterol homeostasis.

Provided are a novel secretion booster and secretion boosting method with respect to extracellular vesicle secretion from cells. The extracellular vesicle secretion booster of the present invention contains an ABCA1 reducing agent. The extracellular vesicle secretion boosting method of the present invention includes boosting extracellular vesicle secretion by causing a target having a cell to coexist with the extracellular vesicle secretion booster of the present invention.

Compositions and methods for diagnosing, treating, preventing, inhibiting, or ameliorating the symptoms of a disease or disorder that is modulated or otherwise affected by ABCA1 levels and cholesterol efflux or in which ABCA1 levels and cholesterol efflux is implicated are disclosed herein. PIP2 is shown to affect ABCA1 levels and promote RCT leading to reductions in unwanted cholesterol levels and atherosclerosis.

The invention provides a new application of a natural metabolite 25-hydroxycholesterol (25-hydroxycholesterol (25 HC for short) in a body to treatment of liver lipid deposition induced by rifampicin (RFP for short), and particularly provides a new application of the natural metabolite 25-hydroxycholesterol (25 HC for short) to treatment of liver lipid deposition induced by rifampicin (RFP for short). The < 25 > HC is a metabolite generated by catalyzing cholesterol by using in-vivo cholesterol 25-hydroxylase (CH25H), and the < 25 > HC is a metabolite generated by catalyzing cholesterol by using the in-vivo cholesterol 25-hydroxylase (CH25H). The compound is reported to have the biological activities of resisting viruses, activating interferon, resisting tumors, participating in lipid metabolism and the like in the past. The invention finds that RFP can induce liver fatty degeneration and lipid droplet deposition and reduce CH25H expression, so that the lack of 25HC may be one of the mechanisms of RFP-induced liver lipid deposition. The invention firstly discovers that the supplement of 25HC can relieve RFP-induced lipid droplet deposition (both triglyceride and cholesterol are reduced), and particularly firstly discovers that the mechanism of reducing the content of cholesterol in the liver by 25HC is related to promotion of expression and entry of LXR alpha into cells and promotion of expression of cholesterol efflux genes ABCA1, 2 and 3. Therefore, the 25HC possibly reduces lipid deposition in the liver by promoting cholesterol excretion of liver cells and relieves the RFP-induced liver injury, and a foundation is laid for future clinical application of the 25HC.

Provided herein are methods of treating a subject having a peripheral nervous system (PNS) myelination condition, comprising administering an effective amount of a pharmaceutical composition comprising a pharmaceutically acceptable carrier and a polypeptide having cholesterol efflux activity, wherein the polypeptide is selected from CS6253 and variants thereof. The PNS myelination condition can be a condition characterized by PMP22 dysfunction in the PNS, a PNS myelination disorder resulting from abnormal ABCA1 regulated cholesterol transport disorder, a demyelinating condition resulting from Schwann cell dysfunction and a non-hereditary PNS myelination condition.

The disclosure relates to an indolo[2′,3′:3,4]pyrido[2,1-b]quinazoline compound represented by general formula (I) and use thereof in the manufacture of (1) a medicament for treating a cardiovascular and cerebrovascular disease, (2) a formulation for increasing expression of AMPK, ABCA1 and SR-BI, (3) a formulation for activating nuclear receptors (NRs), and inhibiting activity of NLRP3, IL-1β, NF-κB and MAPKs, (4) a formulation for promoting cellular cholesterol efflux; or (5) a medicament for anti-inflammation.

The invention relates to the technical field related to biological medicine, in particular to a method for inhibiting cholesterol esterification of macrophages, through targeted regulation of a PPAR-gamma / LXR-alpha signal channel by means of palmatine (PAL), foam cell formation can be effectively reduced, and accordingly atherosclerosis (AS) can be improved. Oxidized low-density lipoprotein (ox-LDL) is used for inducing foaming, then 25-100 [mu] g / ml palmatine is used for intervening for 48 hours, and experiments show that the palmatine remarkably reduces the cholesterol esterification rate (from 52.17% to 41.88%, Plt; according to the present invention, with the application of the palmatine in the preparation of the medicine, the expression of cholesterol efflux genes such as ABCA1, ABCG1 and the like is up-regulated, the release of inflammatory factors IL-6 and TNF-alpha is inhibited (reduced by more than 60%), and the molecular docking proves that the combination of the palmatine and the PPAR-V is stable (the combination energy is-8.482 kcal / mol), and is superior to the traditional medicine; the invention provides a new strategy for natural, safe and multi-target intervention of AS, and has significant clinical application potential.

The invention belongs to the technical field of biological medicines, and particularly relates to application of 4-octyl itaconic acid in preparation of a medicine for preventing and treating AS. In-vivo and in-vitro model research finds that 4-octyl itaconic acid further promotes ABCA1 expression by activating an NRF2-HO-1 / NQO1 antioxidant network, promoting formation of an NQO1-p53 compound, blocking ubiquitination degradation of p53 and improving p53 stability, so that cholesterol excretion of VSMCs is enhanced, formation of foam cells is reduced, and AS plaque lipid deposition is remarkably relieved. The invention systematically reveals the action mechanism of 4-OI in AS lesion for the first time, and provides a new treatment strategy and theoretical basis for early intervention of AS.