28 results about "Tubular cell" patented technology

The present invention aims to provide a cytoprotective agent against ferroptosis that contains DHMBA as an active ingredient, by verifying the effect of DHMBA in suppressing ferroptotic cell death using DN model mice and human renal tubular cells HK-2, for each useful agent containing DHMBA as an active ingredient. [Solution] The present invention provides a cell agent for ferroptosis that has a cytoprotective effect against ferroptosis, comprising 3,5-dihydroxy-4-methoxybenzyl alcohol as an active ingredient.

The invention discloses an application of a targeted ECT2 inhibitor in preparation of a product for treating renal interstitial fibrosis. According to the application, a brand-new and unprecedented molecular pathway which activates a p53 pathway by inhibiting ribosome biogenesis (RiBi) and finally causes renal tubular cell aging and renal fibrosis is revealed and confirmed for the first time, and a solid theoretical basis is provided for precise drugs aiming at the pathway; and a major breakthrough from relevance observation to causality mechanism clarification is realized.

The invention discloses application of a TAX1BP1 function enhancer in preparation of a medicine for preventing or treating acute kidney injury, and belongs to the technical field of biological medicine. The invention also provides a pharmaceutical composition for treating the cisplatin-induced acute kidney injury. The pharmaceutical composition comprises the TAX1BP1 function enhancer and a pharmaceutically acceptable carrier. According to the application, the autophagy process of renal tubular cells can be remarkably activated through lentivirus overexpression TAX1BP1, cell death caused by cis-platinum is reduced, renal function indexes of mice with acute kidney injury (AKI) are improved, and the application provides a new strategy for clinical treatment of chemotherapy-related acute kidney injury.

The invention relates to the technical field of biological medicine, and discloses an activated cis-platinum reversible coordination complex, coordination nano-micelles thereof and application of the activated cis-platinum reversible coordination complex and the coordination nano-micelles. The activated cis-platinum reversible coordination complex is a complex formed by a coordination material and a metal platinum drug or an activated molecule thereof or a derivative thereof, and the coordination ratio of a coordination group in the coordination material to the metal platinum drug or the activated molecule thereof or the derivative thereof is less than or equal to 2: 1; the coordination material is a coordination phospholipid-like material or a coordination polymer material; the metal platinum medicine or the activated molecule or the derivative thereof is cis-platinum, carboplatin, lobaplatin, epithiaplatin, nedaplatin, oxaliplatin or the activated molecule or the derivative thereof. According to the activated cisplatin reversible coordination complex and the coordination nano-micelle and application thereof, the coordination nano-micelle not only can realize cisplatin controlled release regulated by iron ions, but also can reduce ferroptosis of renal tubular cells and related renal cells by chelating the iron ions, so that the renal toxicity of the cisplatin is efficiently inhibited, and the application value is wide.

The present disclosure provides a bioengineered kidney construction method based on organoids and acellular scaffolds, which comprises first injecting pro-vascular stem cells into a kidney acellular scaffold material, and then culturing for several days through fluid circulation perfusion, and then injecting kidney organoids (KIO) into the scaffold material for perfusion culture after the kidney acellular scaffold material is recellularized. The bioengineered kidney obtained by the method of the present disclosure can be used as a graft for replacing kidney function. The present disclosure also provides a kidney organoid culture and expansion method, and the organoids obtained by the method contain not only kidney parenchymal cells such as glomerular cells and renal tubular cells, but also blood vessels and immune cells, which provides a good source of kidney parenchymal cells for the preparation of tissue-engineered kidneys.

The invention provides application of dehydrodiisoeugenol (DHE) to treatment of acute kidney injury by inhibiting ferroptosis, and belongs to the technical field of biological medicine. It is found that DHE can effectively inhibit cell ferroptosis, application of DHE as a ferroptosis inhibitor and application of DHE in preparation of drugs for treating acute kidney injury are provided, and DHE can inhibit renal tubular cell ferroptosis, recover the anti-oxidation defense function and relieve lipid peroxidation and iron deposition. It is proved that DHE is a natural small-molecule inhibitor of ACSL4, ACSL4-mediated ferroptosis can be effectively blocked, powerful protection is provided for cisplatin-induced acute kidney injury, and the DHE becomes a promising treatment candidate drug for cisplatin treatment of patients.

The invention relates to a characteristic gene of senescent renal tubular cell subgroups related to diabetic nephropathy and application thereof, and the characteristic gene and functional difference of each subgroup of senescent renal tubular cells in a renal puncture sample of a patient with diabetic nephropathy are analyzed through single cell transcriptome sequencing and bioinformatics technologies. The four gene segments CXCL8, MMP7, ADIRF and SCL12A1 are screened out to serve as markers for sorting the diabetic nephropathy specific senescent renal tubular cell subgroups, and compared with normal people, the senescent renal tubular cells of diabetic nephropathy patients have high expression of CXCL8 and MMP7 and low expression of ADIRF and SCL12A1, so that the diabetic nephropathy specific senescent renal tubular cell subgroups can be separated from the senescent renal tubular cells of the diabetic nephropathy patients, and the diabetic nephropathy specific senescent renal tubular cell subgroups can be separated from the senescent renal tubular cells of the diabetic nephropathy patients. The development of the diabetic nephropathy from the early stage to the progression stage is stronger; by detecting the level of the markers in the senescent renal tubular cells, the development and prognosis of the diabetic nephropathy can be predicted in an early stage, and potential effective prevention and treatment measures can be provided for delaying the DN development through targeted intervention of senescent renal tubular cell subgroups.

[Problem] The purpose of the present invention is to provide, as each useful agent that contains DHMBA as an active ingredient, a cytoprotective agent against ferroptosis, the cytoprotective agent containing DHMBA as an active ingredient and having a cytoprotective action against ferroptosis by verifying the effect of suppressing ferroptosis cell death of DHMBA using a DN model mouse and a human renal tubular cell HK-2. [Solution] The present invention provides a cell agent against ferroptosis, the cell agent containing 3,5-dihydroxy-4-methoxybenzyl alcohol as an active ingredient and having a cytoprotective action against ferroptosis.

The invention discloses an engineered exosome and a preparation method and application thereof, the exosome comprises a therapeutically effective amount of CD5L protein, and the surface of the exosome is conjugated with kidney targeting peptide LTH which can specifically target injured renal tubular cells. According to the exosome, the exosome containing CD5L is separated from fibrous reticulate cells engineered to overexpress CD5L protein, and then a kidney targeting peptide LTH is conjugated to the surface of the exosome. The exosome can specifically deliver CD5L to injured renal tubules in a targeting manner, kidney tissue injury caused by S-AKI is effectively relieved, and microcirculation disturbance of the whole body is relieved. The invention provides a novel treatment strategy and candidate medicine with targeting and high efficiency for treating acute kidney injury caused by sepsis.

The present invention relates to the fields of nucleic acid drugs and pharmaceutical chemistry, and in particular to a short antisense nucleotide targeting a proximal renal tubule. Provided is an antisense oligonucleotide targeting a proximal tubular cell, or a pharmaceutically acceptable salt thereof. The antisense oligonucleotide has a structure comprising a 5'-wing region, a spacer region, and a 3'-wing region, wherein the 5'-wing region consists of 1-5 nucleotides having a first chemical modification, and the 3'-wing region consists of 1-5 nucleotides having a second chemical modification.

The present invention discloses a biochanin derivative, a preparation method thereof, and its application in a drug for alleviating drug-induced renal injury. The biochanin derivative has the following general formula: wherein R is hydrogen, a linear, branched, or cyclic alkyl group having 1 to 10 carbon atoms, a linear, branched, or cyclic alkyl group having 1 to 10 carbon atoms containing N, O, S, or a halogen, or any one of aromatic hydrocarbons. The biochanin derivative provided by the present invention is non-toxic to renal cells, has strong anti-inflammatory activity, can effectively alleviate the toxic damage of cisplatin to human proximal renal tubular cells HK-2, and significantly improve cisplatin-induced acute kidney injury in mice.

The invention provides a bioengineering kidney construction method based on an organoid and a decellularized scaffold, and the method comprises the following steps: injecting blood vessel promoting stem cells into a kidney decellularized scaffold material, carrying out fluid circulation perfusion culture for several days, and after the kidney decellularized scaffold material is re-cellularized, injecting a kidney organoid (KIO) into the scaffold material for perfusion culture. The bioengineering kidney obtained by the method disclosed by the invention can be used as a graft for replacing renal functions. The invention also provides a kidney organoid culture amplification method, the organoid obtained by the method not only contains kidney parenchymal cells such as glomerular cells and renal tubule cells, but also contains blood vessels and immune cells, and a good kidney parenchymal cell source can be provided for tissue engineering kidney preparation.

The invention relates to the technical field of medical research, in particular to a method for promoting fatty acid degradation and delaying AKI-CKD conversion, which comprises the following steps: a key link of AKI-CKD conversion: peroxisome fatty acid oxidation; the method comprises the following steps of: promoting AKI-CKD transformation by injury of renal tubular epithelial cells (Proximal Tubular Cells, PTCs), and promoting AKI-CKD transformation by injury of the PTCs; the peroxisome FAO affects energy metabolism in PTCs repair; the peroxisome FAO plays a key role in delaying AKI-CKD conversion, and exploration of a regulation and control network mechanism of the peroxisome FAO is very necessary. The application has the advantages that the effect of peroxisome FAO in conversion is focused from the progress characteristic of the AKI-CKD disease, the inhibition of XOR can regulate and control the peroxisome FAO by promoting ABCD3, the regulation and control effect of XOR is preliminarily verified, and a theoretical foundation is laid for subsequently exploring the regulation and control mechanism of XOR; the research preliminarily proves that XOR plays an important role in AKI-CKD disease progression by regulating peroxisome FAO, and provides a new perspective for deeply understanding the pathogenesis of AKI-CKD.

An electrochemical cells and methods of making the same are disclosed. An electrochemical cell may include a cell housing and a cell core. The cell housing may define a tubular cell body extending along a longitudinal axis from a distal end to a proximal end. The cell core may be disposed in the cell housing. The cell core may include a winding core extending along the longitudinal axis, a cathode, an anode, a plurality of inner windings, and a plurality of outer windings. The plurality of inner windings may be coiled around the winding core and define an inner diameter. The plurality of outer windings may be coiled around the plurality of inner windings and define an outer diameter.

Loss of B cell tolerance and generation of autoreactive anti-nuclear antibodies are hallmarks of systemic lupus erythematosus (SLE) and lupus nephritis. Lupus nephritis is characterized by glomerular and tubulointerstitial inflammation often initiated by the renal glomerular deposition of anti-nuclear immune complexes which trigger subsequent activation of complement, macrophages / monocytes and other innate inflammatory cells. The mechanism of anti-nuclear immunoglobulin accumulation and clearance in lupus nephritis pathogenesis remains largely uncharacterized. Here, we show that innate immune activation in the NZB / W F1 mouse model and in human lupus nephritis biopsies rapidly reduces DNase1 expression in renal cortex proximal tubular cells. To overcome the loss of endogenous DNase1, we treated lupus-prone mice with a hyperactive actin resistant variant of DNase1 with improved catalytic activity against nucleic acid-IgG immune complexes and acceptable in vivo pharmacokinetics. Hyperactive DNase1-Fc fusion protein ameliorates nephritis in a murine model of lupus nephritis and reduces immune complex deposition / complement fixation. Taken together, our data suggest that the loss of renal DNase1 through TLR signaling or other innate immune activation impairs clearance of autoreactive anti-nuclear immune complex deposits in the kidney to promote nephritis progression. Our findings provide a therapeutic rationale for using an engineered DNase1-Fc as a potential therapeutic approach in lupus nephritis.

This application provides a wood-based decorative material that has high strength and retains the appearance of wood. The wood-based decorative material comprises wood material and a hydrophobic polymer injected into the wood material, wherein the hydrophobic polymer is in contact with the surface of the cell wall of the tubular cells on the intracellular side when the tubular cells of the wood material have cavities.

The present invention provides a method for histological staining using protein markers and its application in differentiating sieve elements and companion cells, belonging to the technical field of biological histology. The present invention discloses a method for differentiating early tubular cells of sieve elements and companion cells in plant phloem. By using epigenetic protein markers and histological staining, before the nuclei of sieve elements disappear in specific structures, two symbiotic tubular molecules in the phloem, namely sieve elements and companion cells, can be differentiated according to whether the cells are stained. At the same time, the specific location of the interaction between methylated histone and companion cells can be distinguished according to the staining location and depth, and the development degree of companion cells can be evaluated, with high sensitivity and high precision.

The invention discloses a chronic kidney disease glycolysis-immunoregulation analysis method based on multiple omics, which comprises the following steps: acquiring GSE209781 single cell and GSE37171 transcriptome data, and analyzing glycolysis pathway activity and differential genes after preprocessing and cell clustering annotation; molecular subtypes are determined through consensus clustering and immune infiltration assessment; key diagnostic genes such as ETFB and the like are screened in combination with three types of machine learning; molecular docking verifies the binding potential of ETFB and therapeutic drugs. According to the invention, near-end renal tubular cells are positioned as a glycolysis core, an MIF-mediated regulatory network is disclosed, the diagnosis accuracy is improved, a clear treatment target is provided, a standardized analysis system is constructed, and accurate CKD diagnosis and treatment are assisted.

This invention relates to the fields of biomedical engineering and nanomedicine delivery technology, specifically disclosing a homologous membrane nano-targeted drug delivery system for treating acute kidney injury with sepsis. The system includes: preparation of solid silicon spheres; mesoporization and etching; drug loading; preparation of homologous cell membranes; encapsulation and fusion; characterization and quality control. This invention utilizes KTP-modified RBCM vesicles to provide homologous surface proteins / receptors, achieving highly selective recognition and endocytosis of renal tubular cells, significantly improving drug accumulation and bioavailability in diseased kidney tissue, thereby enhancing therapeutic efficacy and reducing systemic exposure. The hollow, mesoporous structure provides high drug loading capacity and controllable release sites. The outer homologous membrane inhibits early leakage under physiological conditions and promotes drug release in inflammatory, acidic microenvironments, or intracellular environments, combining the advantages of sustained release and targeted activation.

The invention relates to application of ginsenoside Ro in preparation of a medicine for preventing and treating kidney stone, and belongs to the technical field of biological medicine. The invention discloses application of ginsenoside in preparation of a medicine for preventing and treating kidney stone. The invention discovers that the ginsenoside Ro has an improvement effect on calcium oxalate (CaOx) crystal deposition, adhesion, renal tubular cell injury and inflammation caused by an ethylene glycol-induced mouse urolithiasis model, and meanwhile, the effect of ZnT1 in renal tubular epithelial cell copper death caused by crystal injury and the copper death resisting effect and mechanism of the ginsenoside Ro are clarified. And a road is laid for novel medicines for treating urolithiasis.

The invention belongs to the technical field of biology, and particularly relates to application of lupeol to preparation of a medicine for preventing or treating renal injury caused by cis-platinum. The invention discovers that the natural compound lupeol has a potential protection effect on the renal injury caused by the cis-platinum for the first time, and in-vivo and in-vitro models prove that the lupeol remarkably relieves renal dysfunction, tissue pathological injury and rising of renal injury markers caused by the cis-platinum, inhibits cell apoptosis and promotes proliferation of renal tubular cells. A transcriptome sequencing result shows that lupeol enhances cell survival and proliferation by activating a PI3K / Akt signal channel, regulates an Nrf2 channel to resist oxidative stress, inhibits nuclear translocation of NF [kappa] B, reduces pro-inflammatory cytokines and inhibits inflammatory response. Results show that lupeol may become a choice for relieving renal toxicity of cis-platinum.

The invention discloses a yang-warming and kidney-tonifying paste patch for preventing diabetes from being converted into diabetic kidney and a preparation method thereof. The traditional Chinese medicine ointment patch is prepared from traditional Chinese medicines such as radix rehmanniae preparata, fructus evodiae, clove, cortex cinnamomi, radix codonopsis, radix puerariae and semen cuscutae, and is prepared by grinding the traditional Chinese medicines into powder, blending the powder into paste and preparing the paste into a cylindrical medicine cake. The traditional Chinese medicine composition acts on the Shenshu acupoint through acupoint application, and traditional Chinese medicine ingredients are used for regulating kidney qi and blood and protecting kidney functions. Clinical tests show that a test group using the application is remarkably superior to a control group in the aspect of improving the traditional Chinese medicine syndromes. The fatty acid binding protein 1 in the early kidney injury marker urine has the effects of regulating lipid metabolism and resisting oxidative stress, can protect renal tubule cells, and has the early kidney injury warning capability, and a test group applying the application has a remarkable effect of reducing the level of the fatty acid binding protein 1. Safety analysis shows that the application is low in adverse reaction occurrence rate and good in safety. The invention provides a traditional Chinese medicine non-drug therapy which has no gastrointestinal burden and is convenient for long-term persistence for preventing and treating the diabetic kidney disease.

The present invention discloses the use of terminalia chebula acid in the preparation of a drug for treating urinary stones. Terminalia chebula acid is an organic acid containing three carboxyl groups (‑COOH) and three hydroxyl groups (‑OH) in its molecular structure. The coordination bond between the carboxylate ion of terminalia chebula acid and the calcium ion can effectively fix the calcium ion to form a soluble complex. The present invention found that terminalia chebula acid at an appropriate concentration or dose showed a good effect in inhibiting the formation of renal calcium oxalate stones. In addition, terminalia chebula acid at an appropriate dose or concentration can significantly alleviate the damage and resulting apoptosis of renal tubular HK‑2 cells caused by oxalic acid and kidney stones.

The invention particularly discloses nanoparticles wrapped by renal tubular epithelial cell membranes as well as a preparation method and application of the nanoparticles, and relates to the technical field of biological medicines. The invention provides nano-particles (FNMs) wrapped by a renal tubular epithelial cell membrane. The nano-particles comprise the renal tubular cell membrane, a contrast agent and a dye. The FNMs can accurately target carotid artery plaques in an APOE <- / -> mouse AS model to realize fluorescence / magnetic resonance bimodal imaging, and lesion information of the plaques can be comprehensively reflected from multiple angles. The defects of low bioavailability of traditional medicine treatment and high trauma risk of traditional surgical treatment are overcome. The PDT effect can be generated under the illumination effect when the concentration is 40 mu g / mL, and the treatment effect of relieving the AS plaque lesion is achieved. No matter in a cell experiment or an animal experiment, the FNMs show high biological safety.

This invention discloses the application of a peptide SRD in the preparation of drugs for treating acute kidney injury, belonging to the field of biomedical technology. In an in vitro H2O2-induced oxidative stress injury experiment on renal tubular epithelial cells, this invention found that peptide SRD treatment significantly reduced the apoptosis rate of renal tubular cells damaged by oxidative stress, promoted ATP production, and restored mitochondrial respiratory chain function. In an animal model of ischemia-reperfusion-induced acute kidney injury, mice with acute kidney injury injected via the tail vein showed significantly decreased serum creatinine and blood urea nitrogen levels. Pathological observation revealed a significant reduction in the degree of renal tubular injury, a lower histological score, and a significant downregulation of KIM-1, an indicator of the degree of renal tubular injury. This indicates that the antioxidant peptide SRD can improve mitochondrial function in renal tubular cells, effectively reduce renal tubular cell damage, promote the repair of renal tubular epithelial cells in acute kidney injury (AKI), effectively improve renal function, and has a good therapeutic effect on acute kidney injury.

Disclosed is a method for treating nephropathy, which comprises targeted delivery of a nucleic acid composition by means of topical administration. Renal tubular cells are transfected with neutral LNPs by means of ureteral retrograde administration, or renal glomerular cells are transfected with positive and neutral LNPs by means of abdominal aorta administration, thereby better targeting renal lesion cells. The mRNA-LNP technology can be applied to the targeted delivery of a kidney-specific cell population by means of the selection of a drug delivery way, thereby achieving therapy for kidney genetic diseases.

The invention belongs to the technical field of biological medicines, and particularly relates to an application of a lactase-like protein (LCTL) as a therapeutic target of a chronic kidney disease renal injury. The invention also provides an application of a medicament for increasing the expression of the LCTL gene or the protein amount of the LCTL in preparation of a medicament for treating the injury of a chronic kidney disease (CKD). The invention further provides an application of the medicament for increasing the expression of the LCTL gene or the protein amount of the LCTL in preparation of a medicament for treating the injury of the CKD. The invention firstly shows that the kidney injury degree of a CKD mouse model can be aggravated by LCTL gene knockout. The overexpression lentivirus is utilized for the first time, the LCTL gene is overexpressed in vivo, and the kidney injury degree of a CKD mouse model can be relieved. The secretory LCTL is synthesized for the first time, and it is proved in vitro that the secretory LCTL relieves the injury degree of renal tubular cells in a disease state. In a word, the invention provides more treatment strategies for the treatment of chronic kidney disease and kidney injury.

A composition comprising citrate and carnitine which activates the production of the protein Klotho by renal tubule cells protecting them, thus reducing the oxidative stress conditions thereof, which can be used for the conservation, perfusion and reperfusion of organs for organ transplants is disclosed. Furthermore, the composition in the liquid and dietary / nutraceutical formulation can be used for reducing the nephrotoxicity induced by iodinated contrast means, antibiotics, NSAIDs 10 or agents that induce oxidative stress.