AI Article Synopsis
- The study aims to assess how doxycycline can reduce chronic heart damage caused by doxorubicin in rats, focusing on its anti-inflammatory properties and ability to inhibit matrix metalloproteinases (MMPs).
- Male Wistar rats were divided into four groups, with some receiving doxorubicin and others receiving doxycycline alongside it, while various heart-related metrics were evaluated.
- The results showed that doxycycline improved heart structure and function affected by doxorubicin, as it reduced heart enlargement, cardiomyocyte hypertrophy, and restored some metabolic enzyme activity, indicating a potential protective role against cardiotoxicity.
Article Abstract
Aim: Evaluate the influence of doxycycline, an anti-inflammatory and matrix metalloproteinase (MMP) inhibitor, on the attenuation of chronic doxorubicin-induced cardiotoxicity in rats.
Methods: We allocated male Wistar rats into four groups: control (C), doxorubicin (D), doxycycline (inhibitor of MMP, IM), and Dox + doxycycline (DIM). Groups IM and DIM received doxycycline (5 mg/kg, IP) once a week for 4 weeks. In addition, 48 h after every doxycycline injection, groups D and DIM received Dox (5 mg/kg, IP). We performed echocardiogram and evaluated TIMP-4 and collagen I protein expression, MMP-2 activity, and oxidative stress and myocardial metabolism.
Results: Doxorubicin promotes left atrium (LA) and left ventricle (LV) dilatation and decreases in LV fractional shortening, which was improved by doxycycline. Moreover, doxycycline attenuated the LV cardiomyocyte hypertrophy and collagen type I expression. Doxorubicin increased phosphofructokinase and decreased beta-hydroxyacyl Co-A dehydrogenase, pyruvate dehydrogenase, citrate synthase, and ATP synthase activity, which was partially attenuated by doxycycline. Lastly, doxycycline improved antioxidant enzyme activity in the DIM group.
Conclusion: Doxorubicin increases oxidative stress and promotes changes in myocardial energy metabolism, accompanied by structural and functional changes. Doxycycline attenuated the doxorubicin-induced cardiotoxicity, at least in part, through changes in myocardial energy metabolism.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9410319 | PMC |
| http://dx.doi.org/10.3390/jcdd9080254 | DOI Listing |
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