4 results about "Healthy donor" patented technology

This invention relates to the application of mitochondrial formulations in the preparation of drugs for treating chronic obstructive pulmonary disease (COPD). The mitochondrial formulations contain active mitochondria isolated from healthy donor cells, with a particle size of 400–1000 nm, possessing normal mitochondrial membrane potential and ATP generation function, and capable of being internalized by mammalian COPD lung epithelial cells. In vitro cell experiments have confirmed that this mitochondrial formulation can repair CSE-induced mitochondrial dysfunction in lung epithelial cells, inhibit mPTP opening, reduce mtDNA leakage into the cytoplasm, thereby blocking the activation of the cGAS-STING signaling pathway and reducing the release of inflammatory factors such as IL-1β and TNF-α. In vivo experiments in COPD mouse models show that tail vein injection of the mitochondrial formulation can effectively accumulate in lung tissue, significantly improving lung pathological changes such as emphysema and collagen fiber deposition in model mice. This invention provides a novel strategy for COPD treatment based on repairing mitochondrial function and intervening in inflammatory signaling pathways.

The present application relates to the application of mitochondrial transplantation preparation in the preparation of a drug for treating non-alcoholic fatty liver disease, wherein the mitochondrial transplantation preparation comprises active mitochondria isolated from healthy donor cells, and has normal membrane potential and mitochondrial respiratory function. In vivo experiments on a non-alcoholic fatty liver mouse model prove that tail vein injection of the mitochondrial transplantation preparation of the present application can effectively reduce the weight of the mouse, improve the fatty liver condition of the mouse, reduce the accumulation of fat in the liver tissue, and at the same time restore the abnormal liver function of the non-alcoholic fatty liver mouse.

The present application belongs to the technical field of biological medicine, and particularly relates to an oral preparation of lipoxygenase of a healthy donor treatment type intestinal flora exosome package and a preparation method and application thereof. The oral preparation of lipoxygenase of a healthy donor treatment type intestinal flora exosome package comprises 0.18-0.78wt% lipoxygenase, 0.24-0.48wt% fucoidan, 1.0-2.0wt% tetrahydropyrimidine and a healthy donor treatment type intestinal flora exosome supplementing to 100% according to weight percentage. The present application adopts an ultrasonic method to prepare the lipoxygenase of a healthy donor treatment type intestinal flora exosome package, uses the treatment type intestinal flora exosome as a natural medicine carrier, successfully solves the technical problem of low oral bioavailability of lipoxygenase, and provides a new effective means for enhancing immunity and preventing and treating tumors.

This application discloses the application of mitochondrial preparations pretreated with lipoic acid and NMN in the prevention and treatment of doxorubicin-induced myocardial injury. This application pre-treats healthy donors with lipoic acid and NMN to obtain functional myocardial mitochondria with significantly enhanced antioxidant capacity and energy metabolism efficiency. These pre-treated mitochondria are then directly injected in situ into the doxorubicin-damaged myocardium, achieving a synergistic effect of "pretreatment enhancement + local transplantation." This results in significantly better outcomes than conventional mitochondrial transplantation or systemic drug administration alone in terms of efficient colonization and functional replacement. By organically combining donor pretreatment with recipient local transplantation, this application effectively overcomes the shortcomings of existing technologies, such as poor targeting and insufficient efficacy, providing a highly efficient, targeted, and synergistic new treatment strategy for doxorubicin-induced acute myocardial injury.