511 results about "Rat model" patented technology

Systemic suppression of the complement system has been shown to be effective to treat inflammatory disease, yet at the potential cost of compromising host defense and immune homeostasis. Herein disclosed are methods for antigen-specific targeting of complement inhibitors that show that complement inhibitors targeted to the proximal tubular epithelium protect against tubulointerstitial injury and renal dysfunction in a rat model of nephrosis. It is shown that appropriate targeting of a systemically administered complement inhibitor to a site of disease markedy enhances efficacy and obviates the need to systemically inhibit complement. Additionally, it is shown by specifically inhibiting the terminal pathway of complement, that the membrane attack complex (MAC) plays a key role in proteinuria-induced tubulointerstitial injury, thus establishing the MAC as a valid target for pharmacological intervention in proteinuric disorders. The disclosed are compositions can be used in methods of treating pathogenic diseases and inflammatory conditions by modulating the complement system.

The invention belongs to the field of animal experiment models, and discloses application of a composite high-fat forage to construct a non-alcoholic fatty liver disease rat model. The high-fat forage is composed of the following raw materials in percent by mass: 77.5% of a rat basic forage, 10% of egg, 10% of coconut oil, 2% of cholesterol, 0.5% of bile salt, and 500mg / kg / d of sodium valproate calculated according to the rat weight. After 8 weeks, rats all have typical non-alcoholic fatty live symptoms, and liver has a lot of fat accumulation along with inflammatory cell infiltration. The model establishing time is short, the success rate is high, and the composite high-fat forage is applicable to pathogenesis research induced by high-fat-diet combined medicines with liver-toxicity side effect, screening of related control measures and efficacy evaluation of treatment medicines.

The invention relates to a method for preparing type-2 diabetes mouse model, which comprises following steps: using streptozocin to make the reaction of islets of pancreas beta cell of new-born mouse to sugar be reduced, injecting treptozocin to weaning mouse to injure islets of pancreas lightly, feeding mouse with high-sugar high-fat food to enable it resist to insulin, and getting type-2 diabetes mouse model. The type-2 diabetes mouse model is characterized by typical symptom of high fasting blood-glucose concentration, high insulinemia, reduced sugar-resistant property and insulin-resistant property. The time for preparing model is shortened and the success rate is high.

Systemic suppression of the complement system has been shown to be effective to treat inflammatory disease, yet at the potential cost of compromising host defense and immune homeostasis. Herein disclosed are methods for antigen-specific targeting of complement inhibitors that show that complement inhibitors targeted to the proximal tubular epithelium protect against tubulointerstitial injury and renal dysfunction in a rat model of nephrosis. It is shown that appropriate targeting of a systemically administered complement inhibitor to a site of disease markedy enhances efficacy and obviates the need to systemically inhibit complement. Additionally, it is shown by specifically inhibiting the terminal pathway of complement, that the membrane attack complex (MAC) plays a key role in proteinuria-induced tubulointerstitial injury, thus establishing the MAC as a valid target for pharmacological intervention in proteinuric disorders. The disclosed are compositions can be used in methods of treating pathogenic diseases and inflammatory conditions by modulating the complement system.

The invention relates to a method for building a spleen-deficiency chronic atrophic gastritis gastric precancerous lesions animal model. The method is based on the existing spleen-deficiency rat model and the existing chronic atrophic gastritis rat model and is used for building the animal model through united copy of free drinking of N-methyl-N '-nitro-N -nitrosoguanidine (MNNG) solution, irregular eating and purgation. The method comprises the following specific steps of: preparing 10mg / L MNNG storage solution by utilizing sterilized tap water, preparing 80 to 200 mug / mL MNNG solution in temporary use to substitute the drinking water to be drunk freely by the rats, and adopting the free drinking of MNNG as the beginning of the modeling; copying a spleen-deficiency syndrome through irregular eating and improved purgation way, feeding the rats on alternate days since the fifth week after the modeling, and utilizing qi-activating decoction for gavage in a dose of 1 to 3ml per rat every day in the seventh weak; and continuing the modeling for 12 weeks. The animal model built through the method is identical to or similar with the clinical syndrome and physical signs of middle-late lesions in chronic atrophic gastritis. After being verified in repeatedly modeling, the method has good repeatability and good stability. The built model is suitable for selecting traditional Chinese medicine for treating the chronic atrophic gastritis through a traditional Chinese medicine spleen treatment method.

The invention discloses a rat-pig intestinal epithelial cell integrated model established by lipopolysaccharide (LPS) stimulation. Bacterial lipopolysaccharide (LPS) has a function in damaging intestinal epithelial barrier, and the integrated model disclosed by the invention aims at identifying whether an antimicrobial peptide Cathelicidin-BF (C-BF) derived from a snake has a protective effect on LPS-induced enteritidis or not. IPEC-J2 is an intestinal epithelial cell line isolated from the porcine jejunum segment and the porcine digestive system is very similar to the human digestive system. By in vivo rat model and in vitro porcine IPEC-J2 cell model, the protective effect of Cathelicidin-BF on impaired LPS-induced intestinal barrier function is tested. The test results show that the Cathelicidin-BF has protective effects on impaired LPS-induced intestinal barrier function and LPS-induced IPEC-J2 cell damage model.

The invention relates to an experimental animal feeding cabin, which is the big and small mice feeding cabin for simulating the symptom of intermittent anaerobic respiration of animal. One side of hypoxia feeding cabin is further connected with a buffering cabin formed from a closed cabin body and a feeding cage track such that the feeding cabin loading the big mouse is timed to stay between the hypoxia feeding cabin and the outside along the feeding cage track so as to simulate the big mouse model of SAS by the long-period intermittent breathing hypoxia gas. There is no need to timely and frequently discharge the nitrogen in the hypoxia feeding cabin, thus, the consumption quantity of the nitrogen is greatly reduced and the experiment cost is reduced by a wide margin.

The present invention relates to a pharmaceutical composition for the treatment of neurodegenerative disorders, comprising an effective amount of a tungsten (VI) compound, preferably tungstate, and more preferably sodium tungstate (Na2WO4). The pharmaceutical composition of the present invention can be used for the preventive and / or therapeutic treatment of neurodegenerative disorders in mammals (including humans), and especially in the preventive and / or therapeutic treatment of Alzheimer's disease and schizophrenia. The effect of sodium tungstate dihydrate on tau phosphorylation was evaluated in rat models of insulin resistance and type 1 diabetes. Therapeutic treatment of Tau-associated diseases from the present invention includes several advantages: GSK3 inhibition; specificity, since it reduces abnormal hyperphosphorylation of tau caused by nerve-specific proteins; efficacy; lack of toxicity; and low price.

The invention relates to the technical field of traditional Chinese medicines, and provides application of quercetin in preparing a medicine for treating polycystic ovarian syndrome. A test is performed on a rat model with polycystic ovarian syndrome by adopting quercetin, and discovers that the quercetin has a remarkable treatment effect and can remarkably reverse insulin resistance. Quercetin does not have liver or kidney toxicity, is small in side effect, has a good clinical application prospect, does not have drug resistance, can avoid operative wounds, and obtains an excellent clinical effect in PCOS (polycystic ovary syndrome) treatment.