Application of CTRP3 to preparation of drugs for preventing and treating cardiac hypertrophy

Abstract

The invention discloses the application of CTRP3 to preparation of drugs for preventing and treating cardiac hypertrophy. A pathologic hypertrophy model of cells is established in the invention, and the pathologic hypertrophy model proves that administration of CTRP3 can lower the expression of cardiac hypertrophy marker molecules and reduce the average surface area of cardiac muscle cells. An in-vivo animal model is also established in the invention, and the in-vivo animal model proves that after administration of CTRP3, the heart-to-body ratio and the lung-to-body ratio of a mouse significantly decrease, the left ventricular systolic function of the heart of the mouse is significantly improved; interventricular septal thickness in a systolic period and left ventricular posterior wall thickness in a diastolic period are significantly reduced; the cross-sectional areas of myocardial cells significantly decrease; the myocardial cells are arranged more closely and regularly; the degreesof myocardial tissue interstitial fibrosis and pericapillary fibrosis are greatly lowered; and thus, it is indicated that CTRP3 has significant prevention effect on pathological cardiac hypertrophy, delays the occurrence of heart failures, and has good clinical application prospects.

Description

technical field [0001] The invention belongs to the technical field of medicine, and specifically relates to the application of CTRP3 for preparing and preventing pathological myocardial hypertrophy and delaying the occurrence of heart failure. Background technique [0002] Under the action of pressure load, inflammation, oxidative stress and other stimuli, the heart produces a series of changes in gene expression, appearance and cardiac function. These stimuli can either directly stimulate cardiomyocyte hypertrophy or activate signaling pathways Induce overexpression of hypertrophy-related genes, causing cardiac hypertrophy. [0003] Pathological myocardial hypertrophy manifests as a significant increase in heart mass and volume, mostly increased thickness in the middle of the posterior ventricular wall and interventricular septum, narrow cardiac chambers, enlarged cardiomyocyte nuclei, increased cell volume, increased diameter or length, and disordered intercellular arrang...

AI Technical Summary

Problems solved by technology

[0006] The second stage is the decompensation period. Although the heart can be hypertrophied compensatoryly under the stimulation of hypertrophic factors to ensure that the blood supply function will not decline, when the stimulating factors continue to exist, the compensatory ability and energy consumption of cardiomyocytes reach the limit. , cardiomyocytes will produce pathological changes, even apoptosis, replaced by proliferating fibrous tissue, the number of cardiomyocytes will decrease, the function will decline, and myocardial fibrosis will aggravate, which will cause irreversible decline in cardiac contraction and pumping function, and eventually lead to heart failure.

At present, there are many drugs used to prevent and treat myocardial hypertrophy, but due to many problems such as specific mechanism of action, drug sources, side effects, etc., it is urgent to explore new safe and effective drugs for the prevention and treatment of myocardial hypertrophy

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