Key result
Empagliflozin ameliorated doxorubicin-induced cardiotoxicity, improved cardiac function, and reduced oxidative stress in rats, potentially by activating the AMPK/SIRT-1/PGC-1α pathway.
Why the study?
The study aimed to probe the functions and possible mechanisms of empagliflozin in doxorubicin-induced cardiotoxicity.
Does empagliflozin attenuate doxorubicin-induced cardiotoxicity in a rat model?
Does empagliflozin attenuate doxorubicin-induced cardiotoxicity in a rat model?
Empagliflozin attenuates doxorubicin-induced cardiotoxicity in rats by improving oxidative stress and energy metabolism, likely via activation of the AMPK/SIRT-1/PGC-1α pathway.
Answers are grounded in this paper and cite their sources.
Suggests cardioprotective potential of empagliflozin vs doxorubicin in rats; leaves open clinical translation pending human data.
We aimed to probe the functions and possible mechanisms of empagliflozin in doxorubicin (Dox)-caused cardiotoxicity. First, a cardiotoxicity rat model was built by continuously injecting Dox intraperitoneally. Then, empagliflozin (30 mg/kg) was gavaged into the rats. Next, echocardiography was utilized for checking the cardiac function of rats, and H&E staining for observing pathological alterations of the myocardial tissues. Besides, biochemical assays and Enzyme-linked Immunosorbent Assay were adopted to detect the creatine kinase isoenzyme (CK-MB), N-terminal pro-brain natriuretic peptide (NT-proBNP), adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) levels in rat serum and superoxide dismutase (SOD), malondialdehyde acid (MDA), and catalase (CAT) in myocardial tissue, respectively. Furthermore, the expression of AMPK/SIRT-1/PGC-1α signaling pathway-related proteins in the myocardial tissues was tested by Western blot. Continuous intraperitoneal injection of Dox greatly elevated left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD), reduced fractional shortening (FS) and ejection fraction (EF), and notably up-regulated CK-MB and NT-proBNP level in rats' serum, thus impairing cardiac function. Empagliflozin treatment could ameliorate myocardial histopathological damage and alleviate cardiac function and tissue damage by down-regulating LVEDD and LVESD, up-regulating EF and FS, and inhibiting CK-MB and NT-proBNP level in serum. Additionally, empagliflozin improved Dox-induced excessive oxidative stress and dysregulation of energy metabolism. Furthermore, empagliflozin activated the AMPK/SIRT-1/PGC-1α signaling pathway in Dox-caused cardiotoxicity rats. In conclusion, in addition to bettering the cardiac tissue and function injury caused by Dox, empagliflozin also improves excessive oxidative stress and energy metabolism. Notably, empagliflozin may exert cardioprotective effects through activating the AMPK/SIRT-1/PGC-1α pathway.
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Meicong Chen (2023) studied Doxorubicin-induced cardiotoxicity. Empagliflozin vs. Doxorubicin alone was evaluated on Cardiac function, myocardial histopathological damage, oxidative stress, and energy metabolism. Empagliflozin ameliorated doxorubicin-induced cardiotoxicity, improved cardiac function, and reduced oxidative stress in rats, potentially by activating the AMPK/SIRT-1/PGC-1α pathway.
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