17 results about "Mouse Kidney" patented technology

The invention discloses a xanthine oxidase inhibitory peptide with a kidney improving function and application thereof, and belongs to the technical field of biological medicines.The xanthine oxidase inhibitory peptide is screened out by conducting enzymolysis, separation and purification on litopenaeus vannamei processing by-products and utilizing a molecular docking technology, the amino acid sequence of the xanthine oxidase inhibitory peptide is Pro-Leu-Gly-Pro-Pro-Pro, and the amino acid sequence of the xanthine oxidase inhibitory peptide is Pro-Leu-Gly-Pro-Pro-Pro. And the half inhibition concentration of the polypeptide is 2.356 + / -0.2448 mM. The xanthine oxidase inhibitory peptide is proved to have an improvement effect on hyperuricemia mice, the improvement effect is mainly characterized by reducing the content of serum uric acid, creatinine and urea nitrogen of the hyperuricemia mice, inhibiting the activity of xanthine oxidase (XOD) in serum and livers of the mice, inhibiting synthesis of uric acid and improving kidney injury of the mice, and Toxinpred prediction shows that the xanthine oxidase inhibitory peptide has the effect of inhibiting the activity of xanthine oxidase (XOD) in the serum and livers of the mice. The xanthine oxidase inhibitory peptide is free of toxic and side effects, so that the xanthine oxidase inhibitory peptide has a wide application prospect in preparation of food or drugs for improving renal functions.

The invention discloses a xanthine oxidase inhibitory peptide with uric acid reducing activity and application thereof, and belongs to the technical field of biological medicines.The xanthine oxidase inhibitory peptide is obtained by conducting enzymolysis, separation and purification on processing byproducts such as litopenaeus vannamei heads and shells with xanthine oxidase inhibitory activity. The xanthine oxidase inhibitory peptide is screened by using a molecular docking technology, and the amino acid sequence of the xanthine oxidase inhibitory peptide is Pro-Pro-Val-Pro-Pro-Pro. The xanthine oxidase inhibitory peptide has an XOD (X-Oxidase) half inhibitory concentration of 3.181 + / -0.1786 mM. The invention further proves that the xanthine oxidase inhibitory peptide has a certain improvement effect on hyperuricemia mice, and the xanthine oxidase inhibitory peptide mainly has the effects of reducing the content of serum uric acid, creatinine and urea nitrogen of the hyperuricemia mice, inhibiting the activity of xanthine oxidase (XOD) in serum and liver of the mice, inhibiting synthesis of uric acid and improving kidney injury of the mice, and the xanthine oxidase inhibitory peptide has a certain improvement effect on the hyperuricemia mice through Toxinpred prediction. The xanthine oxidase inhibitory peptide uric acid reducing peptide is free of toxic and side effects and has a wide market application prospect.

The application discloses application of a rehmannia glutinosa extract in preparation of drugs for treating kidney injury caused by cisplatin. The application of the rehmannia glutinosa extract in preparation of drugs for preventing and / or treating kidney injury caused by cisplatin; a preparation method of the rehmannia glutinosa extract, comprising the following steps: S1, adding water to the rehmannia glutinosa to perform extraction, to obtain a rehmannia glutinosa water extract; S2, adding ethyl acetate to the rehmannia glutinosa water extract to perform extraction, separating ethyl acetate phase and water phase, to obtain the rehmannia glutinosa extract. The application constructs an animal model by inducing mouse kidney injury by cisplatin, and it is found that the rehmannia glutinosa extract obtained by further separating the rehmannia glutinosa water extract by using solvents such as ethyl acetate and ethanol can improve acute kidney injury caused by cisplatin, and the effect is better than that of the rehmannia glutinosa water extract.

This invention belongs to the field of biomedical technology, specifically disclosing the use of neuron-derived neurotrophic factors in the preparation of drugs for the prevention and treatment of kidney stones. Using a glyoxylate-induced mouse model of kidney calcium deposition, this invention demonstrates that neuron-derived neurotrophic factors can significantly reduce kidney calcium deposition, alleviate renal tubular structural damage, and improve renal function indicators. This achieves comprehensive intervention in the entire process of kidney stone disease, from crystal formation to tissue damage to functional abnormalities, exhibiting superior technical effects compared to single stone-dissolving or stone-expelling strategies, and possesses significant application value and clinical translational potential.

The application provides application of a TAS2R4 agonist in preparation of a drug for treating and preventing diabetic nephropathy, and comprises that a bitter taste receptor 4 subtype (TAS2R4) can be used as a drug target point for treating and preventing diabetic nephropathy, and quinine is used as a TAS2R4 agonist. Specifically, mouse diabetic nephropathy induced by a chemical reagent and mouse podocyte cell line MPC cell damage caused by chronic high glucose are taken as research objects, it is found that mouse TAS2R4 agonist quinine has a prevention and treatment effect on diabetic nephropathy, has a protection effect on podocyte loss caused by high glucose, and has an activation effect on mouse kidney TAS2R4 molecular signal, and a possible molecular mechanism is discussed from the aspects of inhibiting NLRP3 inflammasome activation and NF-kappa B signal activation path, and theoretical basis and technical support are provided for prevention and treatment of diabetic nephropathy, other kidney diseases with inactivation of TAS2R4 molecular signal and other diseases by using TAS2R4 agonists including quinine.

The invention belongs to the technical field of cell separation, and particularly relates to a method for separating kidney immune cells, which comprises the following steps: digesting an obtained mouse kidney tissue block in an RPMI 1640 culture medium of fetal calf serum containing collagenase IV and DNAaseI, collecting an upper-layer single-cell suspension after digestion is completed, washing, centrifuging, and discarding supernate, thereby obtaining the kidney immune cells. And centrifuging by a discontinuous Percoll density gradient centrifugation method, and sucking cells of a high interface layer of 40-80% to obtain the mouse kidney immune cells. According to the technical scheme, a three-step optimization scheme of enzyme digestion, room-temperature sedimentation and density gradient separation is adopted, so that when tissues are dissociated in a warm manner, cell damage is greatly reduced, and antigen loss or degradation caused by enzyme activity and metabolism is effectively reduced.

The invention discloses application of polypeptide in preparation of a diabetic nephropathy alleviator, and belongs to the technical field of medicines. The cordyceps sinensis beta-tubulin polypeptide is synthesized by analyzing the structure of the cordyceps sinensis beta-tubulin and selecting amino acid peptide fragments from the 84th site to the 107th site. The apoptosis of the glomerular mesangial cells is induced by using 50 mmol / L of glucose, and meanwhile, the apoptosis of the glomerular mesangial cells induced by high glucose can be relieved by adding the cordyceps sinensis beta-tubulin polypeptide. A treatment test of the cordyceps sinensis beta-tubulin polypeptide on diabetic nephropathy model mice shows that the body mass and fasting blood-glucose levels of the mice in the cordyceps sinensis beta-tubulin polypeptide group are remarkably reduced, the 24-hour urine protein content of the mice is remarkably reduced, and the kidney injury of the mice in the cordyceps sinensis beta-tubulin polypeptide group is remarkably relieved.

This invention has discovered that the pathogenesis of kidney stones is accompanied by a significant increase in the lactation modification level of histidine at position 147 of ALDOB. Furthermore, when histidine at position 147 is mutated, the lactation modification at position 147 of the mutant amino acid disappears. In vivo experiments show that this mutation can significantly inhibit the accumulation of calcium oxalate crystals in mouse kidneys, preventing the occurrence of kidney stones. Based on this, this invention provides a novel agent and pathway for the prevention and treatment of kidney stones.

The invention belongs to the technical field of biological medicines, and relates to application of Kir4.2 in treatment of renal fibrosis. The invention discovers that the expression level of the Kir4.2 protein (formed by KCNJ15 gene coding) in renal tissues of a fibrotic mouse is obviously lower than that of a wild type mouse for the first time, and the difference has statistical significance; moreover, after the Kir4.2 is specifically knocked out of the renal proximal tubule, renal fibrosis under a UUO and FA induction model can be aggravated, and the fibrosis process of human renal tubule epithelial cells induced by TGF-beta1 in vitro can be remarkably reversed by overexpression of the Kir4.2. Therefore, Kir4.2 can be used as a drug, a drug target or a target gene in gene therapy, is applied to prevention, alleviation and treatment of renal fibrosis, and can provide a new strategy for prevention and treatment of renal fibrosis. The invention further provides a construction method of the kidney proximal tubule specificity Kir4.2 knockout animal model, and the constructed animal model can be used for researching renal fibrosis pathogenesis and screening drugs for preventing, relieving or / and treating renal fibrosis and has a wide application prospect.

The mouse kidney transplantation ureter-bladder anastomat comprises a needle tube, a needle tip is formed at the front end of the needle tube, a lead hole is formed in the needle tip, a depth control mechanism is arranged on the outer wall of the needle tube, and the depth control mechanism can control the depth of the needle tip penetrating into the mouse bladder. By adopting the depth control mechanism, an operator can be allowed to preset the puncture depth according to individual differences of mice, so that the risk that seminal vesicles, blood vessels and other visceral organs on the back side of the bladder of the mice are punctured is avoided, and the safety and repeatability of an operation are improved. The invention further discloses a mouse kidney transplantation ureter-bladder anastomosis method.

The application discloses application of shRNA for specifically inhibiting expression of long-chain non-coding RNA AI662270 in preparation of a medicine for treating renal fibrosis or chronic kidney disease. Overexpression of non-coding RNA AI662270 in a mouse kidney can promote occurrence of renal fibrosis of the mouse. Inhibition of expression of lncRNA AI662270 in a ligated mouse kidney can relieve occurrence of renal fibrosis of the mouse, and provides a new target for treatment of renal fibrosis.

COL3A1 as a marker for detecting kidney stones and its application. The application discloses a new use of COL3A1 as a specific detection marker for kidney stones, and a kit, a detection method and application for detecting kidney stones based on the expression level of COL3A1. Through cross-species transcriptome sequencing, qRT-PCR, Western blot and immunofluorescence verification of human kidney stone clinical samples and mouse kidney stone models, it is confirmed that COL3A1 is significantly up-regulated in kidney tissues of kidney stone lesions, and can be used as a molecular marker for distinguishing kidney stone patients from healthy people. The detection method provided by the application has high specificity and sensitivity, and can realize early screening, auxiliary diagnosis, disease monitoring and recurrence risk assessment of kidney stones, and provides a new molecular target and non-invasive detection scheme for clinical diagnosis of kidney stones.

The invention discloses application of catalpol in promoting macrophage IFN-gamma secretion and an application determination method of catalpol, and solves the technical problem of lack of research on effective components based on IFN-gamma tumor immunotherapy, autoimmune disease regulation, vaccine research and development, health care products, immunopotentiators and the like in the prior art. The application comprises application of catalpol in promotion of macrophage IFN-gamma secretion, and a determination method of the application comprises the following steps: step A, preliminary discovery and verification of effects, UUO mouse kidney differential gene analysis and kidney tissue IFN-gamma detection under different catalpol administration conditions; and B, verifying the effect again, namely detecting IFN-gamma mRNA in RAW264.7 cells under different administration conditions of catalpol and / or detecting IFN-gamma mRNA in mouse bone marrow macrophages before and after catalpol administration. The invention discloses the application of catalpol in promoting macrophage IFN-gamma secretion, and the catalpol has wide application prospects in tumor immunotherapy, autoimmune disease immune function regulation, anti-fibrosis, vaccine adjuvant research and development, health care products, immunopotentiators and the like.

The invention discloses a polypeptide compound and medical application thereof. Experimental data shows that the polypeptide compound has a good inhibiting effect on IL-11, has a remarkable effect in a UUO-induced mouse renal fibrosis model, and can obviously inhibit protein and mRNA expression levels of fibrosis factors FN1 and alpha-SMA and mRNA expression of inflammatory factors TGF-beta and TNF-alpha and an injury marker Ngal.

The invention is applicable to the technical field of biomedicine, relates to a construction method and application of a diuretic-resistant cell model, and establishes the diuretic-resistant cell model by using angiotensin II and aldosterone to jointly induce mouse renal manifold M-1 cells. The model is verified by detecting gene and protein expression levels of aquaporin 2, epithelial sodium channel alpha subunit and arginine vasopressin receptor 2. The method is simple to construct and good in repeatability, can truly reflect the pathological characteristics of diuretic resistance, can stably simulate the state of water-sodium retention caused by excessive activation of a renin-angiotensin-aldosterone system, can reproduce the core characteristic of insufficient curative effect of the diuretic, verifies the occurrence effect of the diuretic resistance, and has a good application prospect. And a stable and controllable in-vitro model is provided for researching a molecular mechanism of diuretic resistance and screening prevention and treatment drugs.

The invention provides application of Qixuekang in preparation of a medicine for treating renal fibrosis. Experimental research proves that the Qixuekang administration can remarkably recover the renal function of a mouse with renal fibrosis in senescence-accompanied chronic kidney diseases, reduce the mouse kidney mesenchymal fibrosis level and the levels of fibrosis markers alpha-SMA and Col1, recover the content of reductive glutathione in the mouse, improve the activity of superoxide dismutase and improve the curative effect of the kidney fibrosis in the senescence-accompanied chronic kidney diseases. Therefore, kidney fibrosis phenotypes and fibrosis-related biochemical indexes of mice are improved. Qi-blood Kang can remarkably restore kidney mesenchymal transformation related gene and protein expression, and kidney fibrosis phenotypes in chronic kidney diseases are improved by reducing related inflammatory media; qiwankang can significantly improve mitochondrial membrane potential, increase mitochondrial neogenesis related gene expression and reduce generation of active oxygen.

The application discloses a kind of high-purity mouse kidney microvascular endothelial cell separation culture methods, belong to cell culture technical field.The separation culture method of the application includes the following steps: (1) enzymolysis digestion;(2) multi-stage filtration impurity removal;(3) differential adhesion initial purification and (4) immunomagnetic bead sorting.The application can significantly improve the purity of mouse kidney microvascular endothelial cells by using the strategy of "enzymolysis-differential adhesion-magnetic bead sorting", especially combined with the step of removing fibroblasts by differential adhesion, is the key to obtain high-quality primary cells.The purity of mouse kidney microvascular endothelial cells obtained by the separation culture method of the application can reach more than 95%, and maintains good biological activity, effectively solves the problem of serious cell contamination in the prior art.