Application of compound GB-0139 to medicine for treating myocardial excessive fibrosis after myocardial infarction

Abstract

The invention discloses application of a compound GB-0139 to a medicine for treating myocardial excessive fibrosis after myocardial infarction, and belongs to the technical field of medicines. Through simulated screening and in-vitro verification, the obvious regulation and control effect of the small molecule compound C28H30F2N6O8S, namely GB-0139, on the hyperfunction of cardiac fibroblast mediated by core protein-galectin-3 for promoting myocardial excessive fibrosis after myocardial infarction is basically determined. Through in-vivo experiments, the compound GB-0139 is verified to be capable of directly blocking the activation of a core pathway TGF beta-smad 2 / 3 mediated by the core molecule galectin-3 through combining with a functional group of the core molecule galectin-3 in the fibrosis process so as to improve the myocardial excessive fibrosis after myocardial infarction. The compound GB-0139 has high specificity, does not interfere with a non-related pathway, and has wider applicability compared with the traditional medicine.

Description

technical field [0001] The invention relates to the technical field of medicine, in particular to the application of a compound GB-0139 in the medicine for treating excessive myocardial fibrosis after myocardial infarction. Background technique [0002] The remaining myocardial tissue after myocardial infarction (MI) undergoes continuous changes with myocardial fibrosis as the main pathological process. Early fibrosis helps to control the infarct size and prevent heart rupture, while late ventricular remodeling caused by excessive fibrosis It can affect the systolic and diastolic function of the heart and has the potential to cause malignant arrhythmia. Myocardial fibrosis undergoes a transition from adaptive compensation (early stage) to pathological decompensation (late stage) during MI, and uncontrolled fibroblast phenotype conversion is the key to pathological decompensation of myocardial fibrosis in the late stage of MI. The main reason is that although the fiber repai...

AI Technical Summary

Problems solved by technology

However, how Gal-3 participates in the TGF-β-Smad pathway to regulate excessive myocardial fibrosis in the late stage of MI, that is, the mechanism of participating in the transformation of fibroblast phenotype is still in its infancy.

However, in the background of excessive myocardial fibrosis in the late stage of MI, there are still no relevant reports on the design and screening of highly selective and specific intervention drugs and inhibitors targeting Gal-3 related biological activity targets

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