5 results about "Post myocardial infarction" patented technology

The application relates to the technical field of biological medicine, and discloses medical uses of HSPD1 acetylation modification in prevention or treatment of myocardial infarction. The application first finds that the acetylation level of an HSPD1 protein K352 site is specifically up-regulated in the pathological process of myocardial infarction, and that the heart function after myocardial infarction can be significantly improved by up-regulating the acetylation level of the site, and myocardial fibrosis and myocardial cell hypertrophy can be inhibited; the acetylation level of the site is down-regulated, and myocardial ischemic injury is aggravated, and the heart function is deteriorated. The application confirms that the HSPD1 K352 site acetylation can be used as a new target point for prevention, treatment and auxiliary diagnosis of myocardial infarction, and provides a theoretical basis and experimental basis for research and development of myocardial infarction targeted drugs and gene therapy products.

The application discloses application of harman alkaline in preparation of a medicine for treating and / or preventing myocardial infarction; the application firstly finds that the harman alkaline can be used for treating and / or preventing myocardial infarction. Meanwhile, the harman alkaline can significantly reduce a myocardial infarction area, improve heart function, and promote blood vessel neogenesis in an infarction edge area; and the harman alkaline can also up-regulate protein expression of CD31. In a cell experiment, the harman alkaline can promote HUVEC cell migration and proliferation after H2O2 injury. The application discloses the anti-myocardial infarction effect of the harman alkaline, provides a new medicine for myocardial infarction treatment, and has important clinical application value.

The application discloses a kind of for preventing or treating post myocardial infarction ventricular arrhythmia pharmaceutical composition, the pharmaceutical composition is by everolimus, ethmolam and fluoxetine, belongs to the field of medicine technology.Immunoblotting proves that everolimus, ethmolam and fluoxetine can inhibit fatty acid oxidation protein.In vitro and in vitro cardiac electrophysiology experiment proves that the pharmaceutical composition can effectively reduce post myocardial infarction ventricular arrhythmia susceptibility.TTC staining proves that the pharmaceutical composition can effectively reduce post myocardial infarction myocardial damage area.Based on the above composition in the regulation of post myocardial infarction ventricular arrhythmia susceptibility, it can be further developed in the clinical application of the disease.

This invention belongs to the field of biomedical materials technology and discloses an injectable hydrogel for myocardial infarction repair and its preparation method. The composite material is prepared by reacting a composite system formed from sodium alginate and gallic acid as a carrier with MXene and resveratrol, and the crosslinking agent is magnesium ions. This hydrogel exhibits excellent injectability (shear-thinning properties), biocompatibility, good conductivity, and antioxidant properties. It can be precisely delivered to the myocardial infarction lesion via minimally invasive injection, rapidly gelling after injection. It can effectively remove excess reactive oxygen species at the lesion site, reduce inflammatory response, and promote myocardial cell protection and tissue repair.

This invention discloses the pharmaceutical applications of UGDH in the prevention and treatment of myocardial infarction, belonging to the field of biomedical technology. This invention is the first to demonstrate that UDP-glucose dehydrogenase (UGDH) plays a key regulatory role in the pathological process of myocardial infarction, with significantly upregulated UGDH expression in a myocardial infarction model. Fibroblast-specific knockdown of UGDH significantly improves cardiac function in mice after myocardial infarction, reduces the infarct area, and inhibits myocardial fibrosis and excessive fibroblast activation; overexpression of UGDH significantly worsens the aforementioned pathological phenotypes. This invention clarifies that UGDH can serve as a novel target for the prevention, treatment, and auxiliary diagnosis of myocardial infarction, providing a new direction for the development of gene therapy drugs for myocardial infarction.