57 results about "Lipid deposition" patented technology

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 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.

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 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 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 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 application relates to the biological medical field, in particular to application of a compound in preparation of a medicine for preventing and / or treating non-alcoholic fatty liver disease. The application relates to the use of a compound represented by formula I or a pharmaceutically acceptable salt or ester thereof, or a prodrug in preparation of a medicine for preventing and / or treating non-alcoholic fatty liver disease. The compound has the effect of significantly improving and reducing lipid deposition, inflammation and fibrosis of non-alcoholic fatty liver disease, and has a good application and development prospect.

The invention provides a recombinant human lactoferrin milk tablet with weight losing and blood sugar reducing functions and a preparation method thereof, and belongs to the technical field of dairy product processing. The recombinant human lactoferrin milk tablet disclosed by the invention is prepared from the following components in parts by mass: 95 to 105 parts of recombinant human lactoferrin, 3 to 4 parts of zinc gluconate, 1 to 1.5 parts of vitamin E, 0.03 to 0.04 part of folic acid and 1300 to 1400 parts of milk powder. Experiments prove that the recombinant human lactoferrin milk tablet prepared by the invention can slow down the weight gain of mice and relieve the impaired glucose metabolism capability caused by high fat diet, and meanwhile, the recombinant human lactoferrin can regulate the lipid degeneration of the liver to a certain extent, relieve the lipid deposition of the liver and inhibit fat cell hypertrophy. The recombinant human lactoferrin milk tablet has the weight-losing and blood-glucose-reducing effects for the first time, and has a wide application prospect in the field of weight losing and blood glucose reducing in the future.

The invention relates to the technical field of biology, in particular to application of a Gpr88 gene in treatment and prevention of a non-alcoholic fatty liver disease, the invention reveals that the GPR88 gene is used as a target spot for preventing and treating the non-alcoholic fatty liver disease for the first time, and research finds that deletion of the GPR88 gene can improve sugar tolerance and insulin resistance of a high-fat diet induced mouse, so that the non-alcoholic fatty liver disease can be prevented and treated. The deletion of the GPR88 gene can significantly reduce the weight of the high fat diet induced mouse liver, and the deletion of the GPR88 gene can significantly reduce the lipid deposition of the high fat diet induced mouse liver. The result shows that the GPR88 gene is an effective target for regulating the occurrence of the non-alcoholic fatty liver disease. According to the invention, the biological function of the GPR88 gene is broadened, and a new theoretical basis and a treatment target are provided for preparing medicines for preventing and treating the non-alcoholic fatty liver disease.

The invention relates to the field of medicine application of organic compounds, in particular to application of puerarin-6 ''-O-xyloside in preparation of medicine for treating postmenopausal lipid metabolism disorder. Animal experiments of postmenopausal lipid metabolism disorder mice induced by ovariectomy and high fat diet show that the puerarin-6 ''-O-xyloside significantly reduces the TG, TC and LDL-C levels of the mice, and also increases the HDL-C level; the liver function is improved, the ALT and AST levels are reduced, the balloon-like degeneration of liver cells and the accumulation of lipid droplets in the cells are reduced, and the volume of fat cells is reduced. From the aspect of mechanism, the PPARalpha pathway is activated to regulate and control gene expression related to fatty acid oxidation, so that liver beta-oxidation is promoted, and ectopic lipid deposition is inhibited. Therefore, the puerarin-6 ''-O-xyloside can be used for preparing a PPAR alpha agonist, a medicine for treating postmenopausal lipid metabolism disorder and a medicine for treating dyslipidemia.

The application discloses an antiatherosclerotic polypeptide of Buthus martensii Karsch and application thereof, and belongs to the technical field of traditional Chinese medicinal material polypeptides. The antiatherosclerotic polypeptide of Buthus martensii Karsch is one of peptide segment 1, peptide segment 2, peptide segment 3, peptide segment 4, peptide segment 5, peptide segment 6 and peptide segment 7, and the amino acid sequences are respectively shown in 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 antiatherosclerotic polypeptide screened by the application can significantly reduce oxidation damage and lipid deposition, especially the peptide segment 5; the application provides a theoretical basis for the medicinal development of the antiatherosclerotic polypeptide of Buthus martensii Karsch and reveals the potential antiatherosclerotic mechanism.

The application discloses a tetrahedral framework nucleic acid complex loaded with equol and application of the complex in preparation of a medicine for relieving fatty liver disease. The complex is obtained by stable combination of tetrahedral framework nucleic acid and equol through hydrogen bond and hydrophobic interaction; the equol is loaded on the tetrahedral framework nucleic acid structure, and can be slowly released, so that the bioavailability of the equol is improved, and the problems of poor water solubility and low stability of the equol are effectively overcome. Meanwhile, the complex can inhibit lipid accumulation in HepG2 cells, relieve lipid deposition of liver cells, and reduce accumulation of TG and T-CHO in cells, and can be used for relieving fatty liver, and preparing more and more efficient fatty liver treatment medicines, and has wide application potential in intervention of lipid metabolism disorder and related metabolic diseases.

The invention belongs to the technical field of biological medicines, and particularly relates to application of EPA (eicosapentaenoic acid) plasmalogen in preparation of medicines for improving or preventing diabetic nephropathy, which is characterized by treating diabetic nephropathy mouse models induced by high fat diet and streptozotocin and having insulin resistance and hyperglycemia accompanied by kidney lipid accumulation and glomerular filtration rate reduction, and particularly relates to application of EPA plasmalogen in preparation of medicines for improving or preventing diabetic nephropathy. The treatment effect of the EPA plasmalogen on the diabetic nephropathy is observed; results show that the EPA plasmalogen has obvious effects of improving kidney functions and kidney ectopic lipid deposition on diabetic nephropathy mice induced by high fat diet and streptozotocin, and also has the effects of reducing blood sugar, improving blood fat, reducing insulin resistance and the like. The EPA plasmalogen is used for intervening the diabetic nephropathy for the first time, and an important basis is provided for clinically treating the diabetic nephropathy by using the EPA plasmalogen.

The invention discloses application of methylallyl trisulfide in preparation of a medicine for treating MASLD or heart lipid deposition and fibrosis induced by high fat diet, and belongs to the technical field of medicine. The invention finds that methylallyl trisulfide (MAT) as a novel hydrogen sulfide precursor drug can influence the function of mitochondrial fusion protein (Mfn2) and influence phospholipid exchange and mitochondrial functions, and has the effect of preventing and treating MASLD. Methyl allyl trisulfide is used for treating MASLD or heart lipid deposition and fibrosis induced by high fat diet, and a new choice is provided for treatment of the diseases.

The invention belongs to the technical field of biological medicines, and discloses application of artemisinene with double functions in promoting liver cell maturation and relieving liver lipid metabolism dysfunction. It is found for the first time that ATT can specifically and efficiently promote human hepatic progenitor cell organoids to differentiate into functional mature hepatic cells, the effect of ATT depends on activation of a cAMP-EPAC signal channel, and the action mechanism and effect are remarkably different from those of a DHA-based scheme in the prior art. Meanwhile, the ATT can obviously relieve lipid deposition of liver cells, improve lipid metabolism disorder, effectively relieve liver cell oxidative stress and lipid peroxidation damage induced by lipid deposition, and prevent the cells from triggered apoptosis.

The invention relates to an application of a chicken CISH gene and an encoding protein thereof in regulating and controlling the crude fat content of yolk. The regulation and control mechanism of the CISH gene on the liver and the relation between the CISH gene and the yolk crude fat content are defined, namely, CISH expression is reduced, a GH / PRL-JAK2-STAT5 negative feedback mechanism is weakened, synthesis of substances such as yolk precursors in the liver is enhanced, and then the substances are transported into the yolk through blood, so that the yolk lipid content is increased. The method for verifying the expression quantity of the CISH gene in the laying hen is adopted, and the lipid deposition level in the egg can be simply and rapidly evaluated. The method not only can provide a new thought for researching yolk lipid deposition, but also lays a foundation for increasing the content of crude fat in the yolk in subsequent production practice.

The invention relates to the technical field of bioengineering, in particular to application of an AIFM2 gene in regulating and controlling intramuscular fat deposition of cattle. The invention discloses a function and an application of an apoptosis-inducing factor mitochondrial associated 2 (AIFM2) gene in regulation and control of fat deposition in cattle muscle, and relates to the technical field of biotechnology, biotechnology, biotechnology and application of the apoptosis-inducing factor mitochondrial associated 2 (AIFM2) gene in the regulation and control of fat deposition in cattle muscle, and application of the apoptosis-inducing factor mitochondrial associated 2 (AIFM2) gene. Cell experiments and animal model experiments prove that AIFM2 gene overexpression can significantly promote adipogenic differentiation of fibroblast / fat progenitor cells (Fibroblast-adipogenic progenitor cells (FAPs) of CD3 / CD4 / PDGFR), increase lipid droplet accumulation, and can promote muscle tissue lipid deposition and serum triglyceride content increase in a mouse body; the action mechanism is that the expression of adipogenic differentiation key genes such as PPAR gamma, C / EBP alpha, ADIPOQ, FABP4 and the like is activated on transcription and protein levels, so that fat metabolism and regional deposition are regulated and controlled. The invention proves that the AIFM2 gene can promote the fat deposition in cattle muscle, and provides reference for cattle molecular breeding.

The invention discloses an application of polypeptide in prevention and treatment of plateau hepatic lipid accumulation. The amino acid sequence of the polypeptide is shown as SEQ ID NO.1. The polypeptide effectively blocks abnormal lipid deposition in parenchymal liver cells and macrophages in the plateau low-oxygen environment by competitively inhibiting the function of endogenous CIRP. Animal and cell experiments show that the polypeptide can significantly improve liver fatty degeneration caused by plateau exposure, thereby providing a brand new targeted therapy strategy and drug candidate for prevention and treatment of plateau-related non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC).

The application discloses a focused ultrasound stimulation system and a control method for regulating liver metabolism, and the system comprises a focused ultrasound transducer, a robot positioning module, an image navigation module and a control module. The image navigation module acquires an ultrasound image of a target region, identifies feature points of a hepatic portal region and generates target point coordinates. The robot positioning module carries and moves the focused ultrasound transducer. The control module controls the robot positioning module to dynamically move the focused ultrasound transducer according to the real-time updated target point coordinates, so that the focal domain of the focused ultrasound transducer coincides with the target region, and controls the focused ultrasound transducer to output low-intensity focused ultrasound. The application also provides application of low-intensity focused ultrasound in preparation of a device for treating non-alcoholic fatty liver disease. The system realizes non-invasive physical regulation of liver metabolism, effectively improves lipid deposition and inflammation state, and has the advantages of automation, precision and repeatability.

The application relates to the field of biological medicine, and discloses application of piperidinic acid in preparation of a medicine for preventing and / or treating non-alcoholic steatohepatitis. The application first discovers that piperidinic acid can prevent and / or treat non-alcoholic steatohepatitis. Specifically, the application finds, through non-targeted metabolomics detection, that the content of piperidinic acid in fecal samples of NASH patients and mouse models is reduced, in-vivo experiments show that supplementing piperidinic acid can reduce the serum ALT and AST levels of NASH mice, reduce the content of triglyceride in the liver, and improve the degree of fatty degeneration, hepatocyte ballooning, inflammatory cell infiltration and fibrosis in the liver in histology. In-vitro experiments show that piperidinic acid can improve lipid deposition, inflammatory cell proliferation and fibrosis of liver organoids. Moreover, piperidinic acid is a metabolite of intestinal flora originally existing in a living body, has no obvious toxicity to the living body, is convenient and fast to administer through an oral mode, and can be conveniently obtained as a commercial reagent.

The present application relates to the field of biological medical technology, and particularly relates to application of E3 ubiquitinase inhibitor in non-alcoholic fatty liver related drugs. TRIM23 has a significant influence on non-alcoholic fatty liver disease, and inhibition of expression of TRIM23 at a cell level can improve lipid deposition of hepatocytes induced by mixed palmitic acid and oleic acid; on the contrary, promotion of expression level of TRIM23 can aggravate lipid accumulation of hepatocytes induced by mixed palmitic acid and oleic acid. Therefore, the TRIM23 inhibitor can be used for preparing a drug for preventing or treating fatty liver.