8 results about "Atp production" patented technology

This invention relates to the field of cosmetic compositions, and more specifically to a synergistic anti-aging composition involving energy metabolism and autophagy, its preparation method, and its application. The composition comprises sea buckthorn fruit extract, trehalose, and a cosmetically acceptable polyol carrier. This invention pioneers a betaine-trehalose-NADES extraction system, achieving low-temperature, high-efficiency extraction while preserving the heat-sensitive active ingredients of sea buckthorn. Trehalose possesses both extraction and autophagy activation effects. A selective separation strategy achieves a balance between efficacy, compliance, and process simplicity. The green, circular process reduces costs and is environmentally friendly. Through the synergistic effect of sea buckthorn fruit extract and trehalose, the composition enhances mitochondrial membrane potential, increases ATP production, inhibits excessive activation of the mTOR pathway, and promotes LC3-II conversion, thus synergistically combating skin aging from multiple targets including cellular energy metabolism, signaling pathways, and autophagy.

This invention relates to a mitochondrial composite nanosystem DTPS@Mito targeting lung inflammation, comprising a mitochondrial core and a functionalized lipid material DSPE-TK-PEG2000-SA modified on its surface. DSPE acts as a hydrophobic anchor inserted into the mitochondrial outer membrane, PEG2000 provides hydrophilicity and biocompatibility, ketithiothiol bonds serve as ROS-responsive linkers, and sialic acid targets the head group to specifically bind to E-selectin, which is highly expressed at the inflammatory site. The DTPS@Mito particles have a diameter of approximately 832 nm, maintaining intact mitochondrial morphology and protein composition. In vitro experiments show that it significantly inhibits the expression of inflammatory factors, reduces ROS levels, restores ATP production, and regulates mitochondrial dynamics. In vivo experiments show that it has enhanced retention and accumulation capacity in the lungs of ARDS mice, significantly alleviating lung inflammation, tissue damage, and oxidative stress, and reducing hyaline membrane formation. This invention achieves the synergistic integration of three major functions: mitochondrial transplantation, targeted delivery, and antioxidation, and can be used to prepare drugs for the treatment of acute respiratory distress syndrome.

This invention relates to the field of cell biology, and discloses a culture medium and method for inducing physiological myocardial hypertrophy based on carnosine. The culture medium for inducing physiological myocardial hypertrophy contains carnosine. By introducing an appropriate concentration of carnosine into a cardiomyocyte system, this invention can induce a series of phenotypic changes in cardiomyocytes related to physiological myocardial hypertrophy, including increased cardiomyocyte area, increased mitochondrial number, enhanced oxidative metabolic capacity, and increased ATP production capacity. These changes can improve the energy metabolism level of cardiomyocytes, thus providing a new technical solution for studying myocardial adaptive remodeling.

This invention relates to the field of cell culture technology, and discloses a method for culturing NK cells and its applications. When NK cells enter a hypoxic environment, not only do their cytotoxic activity and proliferative capacity rapidly decline, but they also experience metabolic disorders such as impaired mitochondrial function, insufficient ATP production, and abnormal accumulation of reactive oxygen species (ROS), leading to functional failure and limiting their application in tumor therapy. Existing technologies mainly rely on constant or single-stage hypoxia induction, failing to improve the insufficient hypoxia adaptation of NK cells at the metabolic level. Therefore, this invention provides a method that uses repeated acclimatization culture with gradually decreasing oxygen concentration to allow NK cells to gradually adapt to the metabolic demands of a hypoxic environment. NK cells cultured using this method exhibit a more stable metabolic state and superior cytotoxic activity in a hypoxic environment, significantly enhancing their anti-tumor efficacy and solving the problem of metabolic imbalance and rapid functional loss of NK cells in the hypoxic tumor microenvironment in existing technologies.

This invention discloses the application of NT5C1A as a therapeutic target for myocardial ischemia-reperfusion injury, belonging to the field of biomedical technology. Through proteomics screening and in vitro and in vivo experiments, this invention is the first to discover and demonstrate that NT5C1A is upregulated in the pathological process of MIRI, and is a key upstream factor regulating the AMPK / SIRT1 / PGC-1α signaling pathway. Overexpression of NT5C1A can effectively activate this pathway, synergistically regulating multiple downstream pathological processes: promoting the expression of mitochondrial fusion proteins Mfn-2 and OPA1, inhibiting the expression of the splitting protein DRP1; significantly promoting ATP production and improving energy metabolism disorders; and regulating the balance of apoptosis-related protein Bax / Bcl-2 expression, inhibiting cardiomyocyte apoptosis, ultimately reducing myocardial damage, improving myocardial function, and reducing the infarct area. This invention provides a new target and strategy for the precise intervention of MIRI.

This invention relates to the field of biomedical technology, and more particularly to the use of a combination of RVX208 and temozolomide for the treatment of glioblastoma. It also relates to the use of RVX208 to resensitize temozolomide-resistant cancers to temozolomide treatment. The use of at least one of RVX208, a pharmaceutically acceptable salt of RVX208, a solvate of RVX208, a hydrate of RVX208, a polymorph of RVX208, an isomer of RVX208, a prodrug form of RVX208, and temozolomide in the preparation of a glioblastoma therapeutic agent. RVX208 inhibits the transcriptional activity of various genes related to cell cycle progression and proliferation maintenance by inhibiting BET family proteins or other target molecules, leading to cell cycle arrest, inhibition of cell proliferation, and induction of programmed cell death. RVX208 also interferes with the transcriptional expression of genes related to mitochondrial homeostasis regulation, resulting in a decrease in mitochondrial membrane potential and reduced ATP production, thus enabling RVX208 to disrupt mitochondrial function in GBM cells and produce a synergistic antitumor effect with temozolomide.

The present application relates to an anti-aging composition for improving cardiovascular function and a preparation method and application thereof, and the composition comprises L-ergothioneine, honokiol, quercetin and coenzyme Q10. The present application creatively designs an anti-aging composition for improving cardiovascular aging, which improves cardiovascular aging from four dimensions of "myocardial energy supply + anti-hypertrophy + endothelial protection + anti-oxidation". Coenzyme Q10 can restore myocardial mitochondrial ATP production, honokiol can reverse myocardial hypertrophy through NAD+ deacetylase, quercetin can improve endothelial function and reduce blood pressure, and L-ergothioneine can protect vascular endothelial cells from oxidative damage and inhibit the formation of ox-LDL. Through research, it is found that the four can cooperate and synergize with each other, and can jointly play an excellent role in improving cardiovascular aging, and achieve multiple protection for cardiovascular aging.

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.