Key result
Perindopril treatment significantly improved cardiac function, increased survival (80% vs 65%), and ameliorated myocardial glucose metabolism (SUV 3.85 vs 6.54) in rats with doxorubicin-induced cardiotoxicity.
Why the study?
To observe the effect of perindopril on cardiac function in doxorubicin-induced cardiotoxicity rats and explore the underlying molecular mechanisms.
Does perindopril improve cardiac function in doxorubicin-induced cardiotoxicity rats?
Does perindopril improve cardiac function in doxorubicin-induced cardiotoxicity rats?
Absolute Event Rate: 3.85% vs 6.54%
p-value: p=<0.05
Perindopril improves cardiac function and survival in doxorubicin-induced cardiotoxicity rats, likely by modulating the Ang II/ROS/HMGB1 pathway.
Supports hypothesis of perindopril benefit in doxorubicin cardiotoxicity models; should not change practice pending human trials.
The present study aimed to observe the effect of perindopril on cardiac function in doxorubicininduced cardiotoxicity rats and explore the underlying molecular mechanisms. We constructed a doxorubicin-induced cardiotoxicity rat model (1.0 mg kg -1 , biweekly) for six weeks. Rats in the doxorubicininduced cardiotoxicity group exhibited impaired cardiac function, disorganized sarcomeres and increased levels of brain serum natriuretic peptide, creatine kinase isozyme MB and troponin I. In addition, compared to normal hearts, doxorubicin-induced cardiotoxicity hearts exhibited significantly higher levels of angiotensinogen, angiotensin II (Ang II), angiotensin II type 1 receptor, protein kinase C, reactive oxygen species (ROS), high mobility group box 1 (HMGB1), nuclear factor kappa B, tumour necrosis factor-, interleukin-6 as well as interleukin-1. Positive correlation was found among Ang II, ROS and HMGB1. After treatment with an angiotensin-converting enzyme inhibitor perindopril, cardiac function and inflammation induced by doxorubicin had distinctly improved. Intriguingly, the levels of Ang II, ROS and HMGB1 decreased significantly. Our findings suggest that perindopril improves cardiac function in doxorubicin-induced cardiotoxicity rats, which might be related with Ang II/ROS/HMGB1.
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Shen et al. (2020) studied Doxorubicin-induced cardiotoxicity (n=60). Perindopril vs. Saline was evaluated on Myocardial 18F-FDG uptake (Standard Uptake Value) (p=<0.05). Perindopril treatment significantly improved cardiac function, increased survival (80% vs 65%), and ameliorated myocardial glucose metabolism (SUV 3.85 vs 6.54) in rats with doxorubicin-induced cardiotoxicity.
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