122 results about "Lipid deposition" patented technology

The invention discloses a bionic nano-composite, a preparation method thereof and application of the bionic nano-composite in preparation of a product for treating atherosclerosis, and belongs to the technical field of medicine preparation. The bionic nano compound is a metal nano enzyme Ir-TiO2 coated by an M2 macrophage cell membrane. According to the invention, the surfaces of Ir-TiO2 nanoparticles are coated with M2 macrophage membranes, so that the nanocomposite with a bionic structure is prepared. After intravenous injection, the formed bionic nanocomposite can actively target endothelial cells in atherosclerotic lesions, and release Ir-TiO2 antagonism to endothelial cells in plaques and cytoplasm of inflammatory macrophages. After the Ir-TiO2 reaches the diseased region, the Ir-TiO2 can play an enzyme role to achieve an anti-inflammatory effect, and can promote inflammatory cells such as macrophages and smooth muscle cells at the diseased region to discharge cholesterol, reduce lipid deposition in the cells, reduce the generation of foam cells and promote the growth of plaques. The nanotherapy can effectively prevent the progress of atherosclerosis lesion inflammation and relieve atherosclerosis.

The invention discloses a method for establishing an animal model for age-related retinopathy caused by lipid metabolism disorder, and the animal model is obtained by specifically knocking out Lss genes from mouse retinal pigment epithelium (RPE) cells by means of a CRISPR / Cas9 gene editing technology. The age-related retinopathy model mouse constructed by the invention shows a retinopathy phenotype with retinal lipid deposition and reduced visual function at the age of 5 months, and the retinopathy is further aggravated along with the increase of the age of the mouse and is similar to the phenotype of age-related retinopathy related to lipid metabolism disorder clinically; and an ideal and effective animal model is provided for researching age-related retinopathy.

The invention discloses a traditional Chinese medicine compound oral preparation for treating male oligoasthenospermia, and belongs to the technical field of traditional Chinese medicine preparations. The rhizoma polygonati processed with wine, the prepared rehmannia root and the like are used for nourishing the liver and kidney to consolidate congenital, the codonopsis pilosula, the astragalus membranaceus and the like are used for invigorating spleen and replenishing qi to complement postnatal, the fried cowherb seed is used for activating blood circulation, and the salted semen plantaginis is used for promoting diuresis, so that the problems of insufficient spermatogenesis and low vitality caused by deficiency of the spleen and the kidney are fundamentally solved. Experiments and clinical researches show that the preparation can significantly improve the sperm quantity, activity and activity rate of oligoasthenospermia model mice and patients, the clinical total effective rate reaches 90%, the pregnancy rate reaches 53.3%, and the curative effect is superior to that of Wuzi Yanzong pills in a control group. The action mechanism covers regulation of blood lipid metabolism, improvement of hypothalamus-pituitary-gonad axis functions, repair of testicular seminiferous tubule structural damage and reduction of lipid deposition, and meanwhile, oxidative stress and inflammatory injury are relieved and spermatogenic cell functions are protected by regulating and controlling a PPAR signal channel and inhibiting molecular pathways such as Cga / Sting mediated cell apoptosis.

The invention discloses a scorpion antiatherosclerosis polypeptide and application thereof, and belongs to the technical field of traditional Chinese medicinal material polypeptides. The anti-atherosclerosis polypeptide of the Buthus martensii Karsch is one of a peptide fragment 1, a peptide fragment 2, a peptide fragment 3, a peptide fragment 4, a peptide fragment 5, a peptide fragment 6 and a peptide fragment 7, and the amino acid sequences are respectively shown as SEQ ID NO.1, SEQ ID NO.2, SEQ ID NO.3, SEQ ID NO.4, SEQ ID NO.5, SEQ ID NO.6 and SEQ ID NO.7. The anti-atherosclerosis polypeptide of the Buthus martensii Karsch is an anti-atherosclerosis polypeptide of the Buthus martensii Karsch. The anti-atherosclerosis polypeptide obtained by screening can significantly reduce oxidative damage and reduce lipid deposition, especially peptide fragment 5; a theoretical basis is provided for medicinal development of the scorpion antiatherosclerosis peptide, and a potential antiatherosclerosis mechanism of the scorpion antiatherosclerosis peptide is disclosed.

The invention discloses application of an overexpressed carp lpla gene in regulation and control of expression of cyprinid fish tissue-related genes, and relates to the field of gene engineering, in particular to application of the overexpressed carp lpla gene in regulation and control of cyprinid fish tissue-related genes. The overexpressed carp lpla gene is applied to regulation and control of contents of lipid indexes of total cholesterol TC and triglyceride TG of different tissues of cyprinid fishes. The invention further discloses application of the overexpressed carp lpla gene in regulation and control of fat marker genes lpla, ppar gamma, Fabp3, fast and acaca of livers and muscle tissues of cyprinid fishes. The invention further discloses application of the overexpressed carp lpla gene in regulating and controlling the relative expression quantity of carp liver cell fat metabolism related genes lpla, ppar gamma, Fabp3, fast, acaca, hsl and pnpla2. The overexpressed carp lpla gene can regulate and control lipid deposition in different tissues in zebra fish, and a research model is provided for lpla to regulate and control fat deposition and differentiation. According to the overexpressed carp lpla gene disclosed by the invention, lpla high-expression carp hepatocytes are obtained through a liposome transfection technology, so that fat key gene expression in the carp hepatocytes is changed.

The application discloses application of a compound ZML1 in preparation of a medicine for treating acute drug-induced liver injury. Through in-vivo and in-vitro experiments, it is found that ZML1 can reverse acute liver injury only by acting for several hours, for example, restoring normal morphology of hepatocytes, reducing lipid deposition, rapidly improving damage performance of various transaminases and the like. The treatment effect of the compound ZML1 of the application on various liver injury indexes is superior to that of existing liver-protecting medicines, especially in improving lipid deposition of hepatocytes, and the compound ZML1 shows more excellent curative effect. Therefore, ZML1 has excellent drug property in treating acute drug-induced liver injury and protecting liver, and thus has a wide application prospect.

The invention discloses an MKP7 targeted bionic nanoparticle preparation as well as a preparation method and application thereof. The MKP7 targeted bionic nanoparticle preparation is a bionic nanoparticle siMKP7 (at) NP-M-pHLIP, wherein the bionic nanoparticle siMKP7 (at) NP-M-pHLIP is coated with a macrophage membrane modified by pHLIP and is loaded with siMKP7. According to the preparation, a PLGA-PEI copolymer is used as a carrier core to wrap siMKP7, an outer layer is coated with a macrophage membrane, the surface of the membrane is modified with pHLIP targeting peptide, and spherical nanoparticles with bionic camouflage and pH sensitive targeting delivery functions are constructed. In-vitro experiments show that the nanoparticles can be effectively ingested by macrophages, and macrophage lipid deposition induced by ox-LDL is remarkably inhibited; in-vivo experiments prove that the preparation can be delivered to atherosclerotic plaque parts in a targeted manner, and by inhibiting expression of MKP7 in macrophages, the carotid plaque area is effectively reduced, the serum inflammatory factor level is reduced, and the blood lipid metabolism is regulated, so that development of atherosclerosis is inhibited, and the curative effect of atherosclerosis is improved. A high-efficiency and low-toxicity nucleic acid drug delivery system is provided for treatment of atherosclerosis.

The invention discloses application of Htr2b and an inhibitor thereof in prevention or treatment of chronic kidney diseases, provides application of Htr2b as a drug target in screening of drugs for prevention or treatment of chronic kidney diseases, and further provides application of the inhibitor of Htr2b in preparation of drugs for prevention or treatment of chronic kidney diseases. It is found that after the Htr2b function of DIO mice is inhibited, kidney injury caused by high fat is obviously relieved, the Htr2b inhibitor can inhibit important inflammatory factors MCP-1, IL-1, IL-6 and TNF-alpha and ectopic lipid deposition of the chronic kidney diseases, renal function markers of creatinine, urea nitrogen and UACR of the DIO mice can be obviously reduced, and the Htr2b inhibitor has the obvious effect of preventing or treating the chronic kidney diseases and has a good application prospect. The compound can be used for preparing medicines for preventing or treating chronic kidney diseases.

The research finds that the SUMOylation level of the liver in a clinical specimen and an animal model of the metabolic dysfunction fatty liver disease is obviously reduced. UBC9 is used as the only key E2 ligase for SUMOylation to regulate and control the SUMOylation level. The invention discloses application of a UBC9 gene overexpression preparation in drugs for treating or preventing metabolic dysfunction fatty liver diseases. Through overexpression of liver specificity UBC9 mediated by an AAV adeno-associated virus vector or overexpression of UBC9 in HepG2 cells by a lentiviral vector, lipid deposition of a C57 mouse liver induced by high fat diet and a cell model treated by palmitate can be remarkably improved, and reduction of the SUMOylation level of the mouse liver and the human HepG2 cells under the high fat background can be reversed. Therefore, the UBC9 gene overexpression preparation can be used for developing drugs for treating metabolic dysfunction fatty liver diseases.

The present invention discloses a pharmaceutical composition for treating non-alcoholic steatohepatitis, liver fibrosis and / or liver cirrhosis, which is prepared from the following raw materials in the following weight ratios: 15-50 parts of Astragalus membranaceus, 5-25 parts of turtle shell, 5-25 parts of Angelica sinensis, 10-30 parts of safflower, 10-30 parts of peach kernel, and 1-10 parts of liquorice. The pharmaceutical composition of the present invention for treating non-alcoholic steatohepatitis can reduce serum transaminase, and significantly reduce lipid deposition, liver tissue inflammation and collagen fiber deposition; the composition of the present invention for treating liver fibrosis can significantly reduce liver tissue pathological inflammation and collagen fiber deposition, as well as the numerical values of related indexes such as serum liver function ALT and AST, and at the same time significantly down-regulate the numerical values of related indexes such as serum PⅢP, PCⅣ, HA and LN, significantly inhibit the activation of hepatic stellate cells (HSCs), the central link of liver fibrosis, significantly reduce the activation of NLRP3 inflammasome in liver tissue, reduce HSC autophagy and activation, and has a good therapeutic effect on both liver fibrosis and liver cirrhosis.

The invention relates to the technical field of biomedicine, in particular to application of an E3 ubiquitin enzyme inhibitor in non-alcoholic fatty liver related drugs. The TRIM23 has obvious influence on the non-alcoholic fatty liver disease, and hepatic cell lipid deposition induced by mixing of palmitic acid and oleic acid can be improved by inhibiting expression of the TRIM23 at the cellular level; on the contrary, promoting the expression level of the TRIM23 can aggravate hepatocyte lipid accumulation induced by mixing of palmitic acid and oleic acid. Therefore, the TRIM23 inhibitor can be used for preparing the medicine for preventing or treating the fatty liver.

The invention relates to a traditional Chinese medicine composition for treating non-alcoholic fatty liver disease and non-alcoholic steatohepatitis. The traditional Chinese medicine composition is prepared from the following raw material medicines in parts by weight: 30-90 parts of Chinese yam, 6-18 parts of pericarpium citri reticulatae, 8-24 parts of raw rhizoma atractylodis macrocephalae, 6-18 parts of fingered citron, 15-45 parts of sedum sarmentosum, 8-24 parts of penthorum chinense pursh, 8-24 parts of salvia miltiorrhiza and 8-24 parts of kudzu vine root. The invention also provides application of the traditional Chinese medicine composition in preparation of medicines for treating non-alcoholic fatty liver diseases and non-alcoholic steatohepatitis. According to the invention, the MCD-induced liver tissue injury and lipid deposition can be obviously improved. According to the invention, the mitochondrial injury caused by the non-alcoholic fatty liver injury can be improved.

This invention discloses a biomimetic nanocomposite, its preparation method, and its application in the preparation of products for treating atherosclerosis, belonging to the field of pharmaceutical preparation technology. The biomimetic nanocomposite is an Ir-TiO2 metal nanozyme encapsulated in an M2 macrophage membrane. This invention prepares a structurally biomimetic nanocomposite by coating Ir-TiO2 nanoparticles with an M2 macrophage membrane. After intravenous injection, the formed biomimetic nanocomposite actively targets endothelial cells in atherosclerotic lesions, releasing Ir-TiO2 antagonistically into the cytoplasm of plaque-containing endothelial cells and inflammatory macrophages. Once Ir-TiO2 reaches the lesion site, it exerts an enzymatic effect to achieve anti-inflammatory activity and promotes cholesterol excretion from inflammatory cells such as macrophages and smooth muscle cells at the lesion site, reducing intracellular lipid deposition, reducing foam cell formation, and promoting plaque growth. This nanotherapy can effectively prevent the progression of inflammation in atherosclerotic lesions and alleviate atherosclerosis.

The invention belongs to the technical field of experimental animal models, biomedical research and immunology, and discloses a photocoagulation thymus ischemia animal model, a method and application of the photocoagulation thymus ischemia animal model in rapid simulation of thymus degeneration and immune senescence, and the model shows at least one or more characteristics 1-7 days after induction: thymus atrophy, thymus weight or thymus index is significantly reduced; the cortical-medullary structure of thymus is disordered or disappears; the expression distribution of the Keratin 5 / Keratin 8 is abnormal; thymic cell apoptosis is increased, and lipid deposition is enhanced; the proportion of CD4 + CD8 + double positive T cells is reduced, and the proportion of DN2 / DN3 stage T cells is increased; the initial T cell output is reduced; and the immune function is reduced. The pathological mechanism is clear; the modeling period is short, and the immune senescence phenotype can be stably obtained within several days; the injury focus is controllable, and systemic stress or hormone interference is avoided; the model has high repeatability and is suitable for mechanism research and drug screening.

The invention discloses application of rebaudioside B in preparation of a medicine for preventing and treating metabolism-related osteoarthritis, and belongs to the technical field of biological medicine. Animal experiments prove that the application of the natural micromolecular monomer rebaudioside B in preventing and treating osteoarthritis induced by high fat diet shows that the rebaudioside B can realize a cartilage protection effect by improving lipid deposition, regulating inflammatory response and promoting cartilage matrix synthesis; the method is suitable for intervention and prevention and treatment of metabolism-related osteoarticular diseases. The invention provides a set of intervention scheme with clear structure, multi-target action, clear mechanism and controllable path for the prevention and treatment of metabolism-related osteoarthritis, and provides a scientific basis for the application of rebaudioside B in the prevention and treatment of metabolism-related osteoarthritis.

The invention discloses application of a lipid synthesis inhibitor in treatment of breast cancer. Researches prove that F.n colonization exists in breast cancer tissues, and the F.n can regulate and control lipid deposition related gene expression and lipid metabolism change of tumor-related macrophages, so that lipid deposition of the macrophages and proliferation, invasion and migration capabilities of tumor cells are promoted; after the lipid deposition inhibitor is added, the lipid metabolism disorder of the tumor-associated macrophages can be inhibited, the tumor malignant phenotype is finally inhibited, and the treatment of the breast cancer is realized. The invention provides a new potential therapeutic target and a new therapeutic drug for effective treatment of breast cancer.

The invention discloses a novel medical application of Chiglitazar, Indeglitazar and LZ03, and belongs to the technical field of medicines. The invention relates to a novel medical application of Chiglitazar, Indeglitazar and LZ03. The new application of the medicine specifically refers to application of a PPAR universal agonist Chiglitazar, Indeglitazar, LZ03 or pharmaceutically acceptable salts thereof to preparation of a medicine for preventing and / or treating Duchenne muscular dystrophy, Duchenne muscular dystrophy skeletal muscle lipid ectopic deposition and Duchenne muscular dystrophy skeletal muscle aplastic disorder. The invention further relates to a preparation method of the medicine for preventing and / or treating the Duchenne muscular dystrophy skeletal muscle aplastic disorder and the application of the PPAR universal agonist Chiglitazar, Indeglitazar, LZ03 and the pharmaceutically acceptable salts thereof. It is proved for the first time that the three compounds can effectively improve core pathological injuries of Duchenne muscular dystrophy, relieve muscle fiber necrosis, skeletal muscle lipid accumulation and aplastic disorder, remarkably improve the skeletal muscle function, fill the application blank of the compounds in the field of Duchenne muscular dystrophy treatment, and have broad application prospects in treatment of Duchenne muscular dystrophy. A brand new candidate drug and a treatment thought are provided for prevention and / or treatment of Duchenne muscular dystrophy, and important clinical application value is achieved.

The invention discloses application of physcion in preparation of a medicine for reducing liver cell lipid deposition, and particularly relates to application of physcion in preparation of a medicine for preventing and treating lipid deposition fatty liver. In-vitro cell experiments prove that the physcion shows low toxicity and a wide safety range in a human normal hepatocyte line THLE3, a human hepatoma cell line HepG2 and a mouse normal hepatocyte line AML12, and can obviously reduce the level of oleic acid-induced intracellular triglyceride in a dose-dependent manner, so that the physcion can be used for preparing a medicine for treating liver cancer. Oil red O staining results also visually show that lipid droplet accumulation in cells can be effectively reduced; according to the invention, the technical prejudice that the emodin monomethyl ether is regarded as a potential hepatotoxic component in the prior art is overcome, a safe and effective new choice is provided for the treatment of the lipid deposition fatty liver, and the pharmaceutical composition has a wide clinical application prospect.

This invention discloses a method for evaluating the bioavailability of soybean oil based on an in vitro digestion / cell co-culture model. Soybean oil is emulsified using WPI emulsifier and then digested sequentially through simulated gastric and intestinal fluids to obtain the gastric digestion products of soybean oil. Fatty acids are extracted from the intestinal digestion products of soybean oil, dissolved in dimethyl sulfoxide, and linked to fatty acid-free bovine serum albumin to obtain in vitro digestion products of soybean oil that can be absorbed by the intestines. These are then added to a cell co-culture model for cell incubation and transport. HepG2 cells from the cell co-culture model are collected, and Oil Red O staining and total triglyceride content are measured to obtain lipid deposition, thereby evaluating the bioavailability of soybean oil. The in vitro digestion / cell co-culture model of this invention is specifically designed for soybean oil digestion. This method objectively and scientifically evaluates the bioavailability of soybean oil at different metabolic stages, providing a standard basis for the scientific and healthy consumption of soybean oil and possessing significant practical value.

The invention relates to application of cepharanthine in preparation of medicines for preventing or treating metabolic dysfunction related fatty liver diseases (Metabolic-associated fatty liver diseases), and particularly relates to application of cepharanthine in preparation of medicines for preventing or treating metabolic dysfunction related fatty liver diseases (Metabolic-associated fatty liver diseases). The invention relates to an application of MASLD in a medicine, and belongs to the technical field of biological medicines. In an in-vivo experiment, a mouse MASLD model is established by adopting methionine choline deficiency diet induction, and the treatment effect of cepharanthine on MASLD is researched. Experimental results show that the cepharanthine can significantly reduce the levels of triglyceride, glutamic-pyruvic transaminase, glutamic oxalacetic transaminase and other indexes of MASLD mice; a pathological detection result shows that cepharanthine can effectively reduce liver lipid deposition and inflammatory infiltration. In-vitro experiments prove that cepharanthine can effectively reduce the content of free fatty acid (Free Fatty Acid); fFA (Fatty Acid) induced HepG2 (HepG2) cell lipid accumulation and lipopolysaccharides (lipopolysaccharides) induced HepG2 cell lipid accumulation and lipopolysaccharides (FFA) induced HepG2 cell lipid accumulation; the THP-1 cell inflammatory response is induced by LPS (Lipopolysaccharide). In conclusion, the cepharanthine shows remarkable anti-lipid accumulation and anti-inflammatory effects in in-vivo and in-vitro experiments, can be used for preparing the medicine for preventing or treating MASLD, and has a wide application prospect.

This invention discloses a method and application for regulating fatty liver syndrome based on osteocalcin-adiponectin receptor, relating to the field of livestock and poultry metabolic disease prevention and control technology. The method includes the following steps: clarifying the clinical symptoms and pathological changes of fatty liver syndrome in laying hens; constructing a complementary validation system for fatty liver syndrome models, including an in vivo FLS model in laying hens and an in vitro LMH model of chicken liver cancer cells; using osteocalcin OCN and the adiponectin receptor agonist AdipoRon to target and intervene in the in vivo FLS model and the in vitro LMH model of chicken liver cancer cells, and conducting multi-dimensional detection and evaluation of the regulatory effect; by specifically silencing the expression of AdipoR1 or AdipoR2, comparing changes in lipid deposition and signaling pathways in cells treated with osteocalcin, and identifying the functional hierarchy of AdipoR1 and AdipoR2 in the osteocalcin regulatory pathway; this invention achieves precise prevention and treatment of fatty liver syndrome in laying hens through complementary validation models, targeted intervention with osteocalcin and AdipoRon, and identification of adiponectin receptor function.

This invention provides the application of Lactaroviolin, derived from macrofungi of the genus *Lactarius*, in the preparation of products for treating MASLD, belonging to the field of biopharmaceutical technology. The key technical point is the application of Lactaroviolin or its derivatives as the main component in the preparation of products for treating MASLD; wherein the products for treating MASLD contain Lactaroviolin or its derivatives as the main component. This invention utilizes Lactaroviolin to significantly reduce lipid deposition, glucose tolerance, and insulin resistance in the liver of HFD mice, thereby treating MASLD. Therefore, Lactaroviolin holds promise for development as a biopharmaceutical formulation for treating MASLD.

The invention relates to the field of biological medicines, and discloses application of piperidine acid in preparation of a medicine for preventing and / or treating non-alcoholic steatohepatitis. The invention discovers that the piperidine acid can prevent and / or treat the non-alcoholic steatohepatitis for the first time. Specifically, non-targeted metabonomics detection finds that the content of the piperidine acid in an excrement sample of an NASH patient and a mouse model is reduced, and in-vivo experiments show that supplement of the piperidine acid can reduce the levels of ALT and AST in serum of an NASH mouse, reduce the content of triglyceride in the liver, and improve the expression of the NASH mouse. And the fat change, liver cell balloon-like change, inflammatory cell infiltration and fibrosis degree in the liver are improved in histology. In-vitro experiments show that piperidine acid can improve lipid deposition, inflammatory cell proliferation and fibrosis of liver organs. Moreover, the piperidine acid is an intestinal flora metabolite originally existing in a living body, and has no obvious toxicity to the living body; the oral administration is convenient and fast; commercial reagents are available and can be conveniently obtained.

The invention relates to the field of traditional Chinese medicine compositions, and particularly discloses a traditional Chinese medicine composition for detoxifying, dredging collaterals, eliminating paste and stabilizing sugar and a preparation method thereof. The traditional Chinese medicine composition is prepared from the following raw materials in parts by weight: 7 to 15g of rhizoma coptidis, 6 to 10g of wine-treated rhubarb, 15 to 30g of radix astragali seu hedysari, 12 to 15g of radix salviae miltiorrhizae, 12 to 20g of radix paeoniae rubra, 6 to 10g of radix bupleuri, 6 to 10 parts of herba artemisiae scopariae, 7 to 15 parts of fructus crataegi and 7 to 15 parts of pericarpium citri reticulatae. The detoxifying, collateral dredging, ointment eliminating and sugar stabilizing traditional Chinese medicine composition can achieve the effects of reducing blood sugar fluctuation and lipid deposition on the basis of achieving the effects of reducing blood sugar and improving the insulin resistance level, can effectively reduce the dosage of compound medicine for a patient so as to improve the compliance of the patient, is safe and effective, delays the occurrence of diabetes complicated diseases and complications, and has a wide application prospect. And the living quality of the patient is improved.

The application belongs to the technical field of traditional Chinese medicine exosomes, and particularly relates to mulberry-derived extracellular vesicle particles, a preparation method thereof and application thereof in the preparation of medicines for preventing and treating hyperlipidemia and related symptoms. The mulberry-derived extracellular vesicle particles provided by the application are prepared by using mulberries as raw materials, centrifuging the mulberries at different centrifugal speeds after juice extraction, and then performing density gradient centrifugation with a sucrose solution with a specific density. Experimental research shows that the mulberry-derived extracellular vesicle particles can significantly reduce total cholesterol, triglyceride and low-density lipoprotein in blood, inhibit the formation of aortic plaques caused by hyperlipidemia and lipid deposition in the liver, and are safe and non-toxic, and therefore can be used for the preparation of medicines for preventing and treating hyperlipidemia and related symptoms.

The invention discloses application of lncRNA in preparation of a product for diagnosing / preventing / treating a non-alcoholic fatty liver disease. The lncRNA is lncRNA Gm34654, and the sequence of the lncRNA is shown as SEQ. ID NO.1. The invention also discloses application of the lncRNA in preparation of a product for diagnosing / preventing / treating the non-alcoholic fatty liver disease. The expression of the lncRNA Gm34654 in a non-alcoholic fatty liver disease mouse model and a cell model is reduced, and the lncRNA Gm34654 has the function of reducing the oxidative stress level and mitochondrial damage in the non-alcoholic fatty liver disease; the research on the lncRNA Gm34654 in a non-alcoholic fatty liver disease mouse model and a non-alcoholic fatty liver disease cell model shows that the lncRNA Gm34654 can improve cell injury and lipid deposition in the non-alcoholic fatty liver disease, which indicates that the lncRNA Gm34654 plays a key role in the pathogenesis of the non-alcoholic fatty liver disease; therefore, the compound can be used for preparing related products for diagnosing / preventing / treating the non-alcoholic fatty liver disease.

The invention relates to an anti-inflammatory and lipid-lowering-based nano preparation for treating fatty liver and a preparation method of the nano preparation. Galactose modified polyethylene glycol-polylactic acid-glycolic acid copolymer (PEG-PLGA) is used as a targeting carrier, and a lipid-lowering drug fenofibrate and an anti-inflammatory drug curcumin are co-loaded; the particle size of the nano preparation is 150-200nm, and the drug encapsulation efficiency is greater than or equal to 85%. Galactose modified PEG-PLGA is adopted as a carrier, galactose can be specifically combined with an asialoglycoprotein receptor (ASGPR) specifically expressed on the surface of liver cells, active targeting of the liver is achieved, the drug enrichment amount of the liver lesion position is remarkably increased, meanwhile, accumulation of drugs in extrahepatic tissue is reduced, extrahepatic toxicity is effectively reduced, and the drug delivery effect is improved. According to the present invention, the anti-inflammatory drug curcumin and the fenofibrate are combined, such that the biological safety of the preparation is improved, the lipid lowering drug fenofibrate and the anti-inflammatory drug curcumin are innovatively co-loaded, and the fenofibrate and the anti-inflammatory drug curcumin form the synergistic effect system: fenofibrate can activate peroxisome proliferator-activated receptor alpha (PPAR alpha), promote liver lipid catabolism, and reduce lipid deposition;

The invention discloses application of a compound with a formula I or a salt, a stereoisomer, a tautomer, a deuterated compound, a solvate, a metabolite, a prodrug or a mixture thereof in preparation of drugs for preventing and treating non-alcoholic fatty liver diseases. The compound disclosed by the invention can be used for remarkably inhibiting lipid deposition in AML12 cells induced by free fatty acid, improving fatty degeneration of liver cells, obviously relieving ballooning and reducing inflammatory cell infiltration. # imgabs0 #

The present invention provides the use of Caspase8 in the preparation of a medicament for non-alcoholic fatty liver disease. Overexpression of Caspase8 inhibits the development of non-alcoholic fatty liver disease. The present invention identifies a specific role of Caspase8 in non-alcoholic fatty liver disease: decreased Caspase8 expression in hepatic macrophages activates the Cflip / ELK4 / Psap signaling pathway, leading to macrophage polarization toward the M1 type. This, in turn, activates the Rac1 / cdc42 / JNK signaling pathway within hepatocytes through the Gpr37I1 receptor on the hepatocyte surface, leading to increased lipid deposition in hepatocytes. Caspase8 or its small molecule analogs may offer hope for the treatment of steatohepatitis.

The present invention discloses an anti - pyroptosis polypeptide and its application, relating to the technical field of biomedicine. The key points of its technical solution are: the anti - pyroptosis polypeptide is specifically used in the preparation of drugs for preventing and treating atherosclerosis. The amino acid sequence of the anti - pyroptosis polypeptide is shown as SEQ ID NO.1. The present invention firstly uses the anti - pyroptosis polypeptide to prepare drugs for treating and / or preventing atherosclerosis, and the effect of the anti - pyroptosis polypeptide in controlling atherosclerosis has been verified in cell models and animal models. In particular, the anti - pyroptosis polypeptide can enhance the viability of endothelial cells in the state of defective pyroptosis, significantly inhibit the expression of pyroptosis - related genes and proteins, and at the same time can reduce the levels of serum cholesterol and low - density lipoprotein in atherosclerotic mice, and reduce aortic lipid deposition and plaque formation. Moreover, when the anti - pyroptosis polypeptide of the present invention is used as a drug ingredient, it also has advantages such as low toxicity, small molecular weight, low immunogenicity and high druggability.