Abstract

Adriamycin (ADR) is an anthracycline antibiotic with the advantages of wide anti-tumor spectrum and strong anti-tumor activity. It is one of the most effective anti-tumor drugs at present, and is widely used in the treatment of leukemia and various entities. Tumor. However, cardiotoxicity of doxorubicin can lead to irreversible myocardial damage, ultimately leading to dilated cardiomyopathy (DCM) or congestive heart failure (CHF). Therefore, to explore the mechanism of ADR-induced myocardial injury, and to find effective and effective protective drugs for the clinical expansion of doxorubicin application range is of great significance. We simulated the ADR myocardial injury model by in vivo and in vitro, and the degree of damage of cardiomyocytes by ADR was observed by detecting the corresponding biochemical indicators and tissue staining. And the expression levels of oxidative stress and inflammatory factors were detected by Western blotting and others methods. Beta-casomorPhin-7 can alleviate myocardial damage caused by ADR, inhibit the expression of oxidative stress and inflammation-related factors, and activate TLR4-MyD88-NF-κB signaling pathway. β-CM-7 inhibits ADR-induced cardiomyocyte oxidative stress and inflammatory responses by activating the TLR4-MyD88-NF-κB signaling pathway. This will provide a new intervention target for the treatment of DCM.

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