6 results about "Kidney ischemia" patented technology

The invention discloses application of a BTK inhibitor in preparation of a medicine for treating acute kidney injury and complications thereof. The invention provides a new strategy for treating acute kidney injury and complications thereof by using a BTK inhibitor, and particularly relates to application of the BTK inhibitor as an acute kidney injury medicine. The invention finds that serum creatinine and urea nitrogen levels can be effectively reduced by knocking out mouse BTK, and kidney injury is relieved and conversion from AKI to CKD is delayed or prevented by recovering kidney pathological structure and reducing apoptotic cell generation, which indicates that BTK is an effective target for treating acute kidney injury. Meanwhile, through treatment of an acute renal ischemia-reperfusion model, it is found that the BTK inhibitor such as ibrutinib can relieve ischemia-reperfusion induced renal function impairment and improve the renal function of a mouse, and it is indicated that the BTK inhibitor can serve as a treatment scheme for acute renal injury.

This invention discloses butylphthalide nanoparticles, comprising: a layered double hydroxide and butylphthalide, wherein the butylphthalide is loaded onto the layered double hydroxide. This invention also discloses a method for preparing the above-mentioned butylphthalide nanoparticles, comprising the following steps: mixing the layered double hydroxide, butylphthalide, and water, adsorbing, separating the solid and liquid phases, and drying to obtain butylphthalide nanoparticles. This invention further discloses the application of the above-mentioned butylphthalide nanoparticles in the preparation of drugs for treating acute renal ischemia-reperfusion injury. This invention also discloses a drug for treating acute renal ischemia-reperfusion injury, comprising: the above-mentioned butylphthalide nanoparticles and pharmaceutically acceptable excipients. The butylphthalide nanoparticles of this invention have high drug loading capacity, good stability, and can target and activate the PI3K-AKT signaling pathway, effectively inhibit HK-2 cell apoptosis and oxidative stress, restore mitochondrial function, and improve renal ischemia-reperfusion injury.

This invention discloses the application of quinolinic acid in the preparation of drugs for the prevention and treatment of acute kidney injury (AKI). AKI refers to acute kidney injury induced by renal ischemia-reperfusion. The drug is an oral formulation used for prophylactic administration in high-risk individuals undergoing iatrogenic procedures at potential AKI risk, and for pretreatment of ischemic conditions in transplanted kidneys. Experiments have shown that administration of quinolinic acid significantly reduces serum urea nitrogen levels in AKI mice, alleviates renal tissue morphological damage in AKI mice, and reduces the expression level of the renal tubular injury factor NGAL protein in AKI mice, demonstrating significant clinical value in the prevention and treatment of AKI.

The invention relates to the technical field of biological medicine, and particularly discloses a platelet membrane-coated mitochondrial compound and a preparation method and application thereof, and the platelet membrane-coated mitochondrial compound comprises mitochondria extracted from mammalian tissues and a platelet membrane coating the outer layer of the mitochondria. According to the present invention, the high kidney injury targeting enrichment rate is achieved through the PMITO compound constructed by coating the mitochondria with the platelet membrane, the healthy mitochondria is accurately delivered to the focus, and the energy crisis and the cell apoptosis are directly reversed; meanwhile, the biomimetic membrane structure can actively adsorb key inflammatory factors such as TNF-alpha and IL-1beta to synergistically realize dual mechanisms of energy repair and inflammation regulation, so that renal function indexes are remarkably improved in an animal model, and tissue pathological damage is relieved; finally, a new strategy for treating the renal ischemia-reperfusion injury, which is high in targeting property, clear in curative effect and good in biological safety, is formed.

This invention discloses a renal hemoperfusion device for use before renal ischemia, relating to the field of perfusion devices. It includes a housing with a pair of fasteners on its side for securing a syringe to each; a movable plate, mounted within the housing via a moving mechanism that drives the movable plate to move within the housing; and a pair of pushers, both mounted on the movable plate, for pushing the piston handle in the syringe. Each pusher includes a sliding sleeve, a moving sleeve, and an elastic member. The sliding sleeve is located on the side of the movable plate, and the moving sleeve is slidably inserted into the sliding sleeve. The advantages of this invention are: strict separation of the two stages avoids human timing errors during operation, ensuring perfusion only after blood vessel closure; the mechanical interlocking mechanism between the baffle and the travel strip forces perfusion to begin only after the fluid-filled bladder has fully expanded, eliminating the risk of misoperation at the hardware level; seamless switching between the injection expansion and perfusion stages ensures high efficiency; and the mechanically pushed perfusion speed during perfusion is more uniform, resulting in better efficacy.

This invention discloses a fluorescent probe for the specific detection of fatty acid amide hydrolases, its preparation method, and its applications, relating to the field of biomedical detection technology. The probe, named TMBID, has the structure shown in formula (I): (I). The structure includes a FAAH-specific recognition unit and a large Stokes shift red fluorophore. This probe has been demonstrated for the first time to selectively and sensitively visualize FAAH activity in renal cell carcinoma cells (ACHN, A498) and a renal ischemia-reperfusion injury (RIRI) model. In vitro experiments showed that TMBID's response to FAAH is not interfered with by other hydrolases (such as FAP-α, aminopeptidase N, etc.), and the URB597 inhibitor significantly suppressed the fluorescence signal by 67%. In cell experiments, TMBID could distinguish renal cell carcinoma cells (high fluorescence intensity) from normal kidney / hepatocytes (fluorescence intensity as low as 20%). Animal models confirmed its specific enrichment in renal cell carcinoma and RIRI tissues. This probe provides a revolutionary tool for early diagnosis of renal cell carcinoma, dynamic monitoring of renal injury, and FAAH-targeted therapy.