Key result
Paricalcitol and vitamin D3 pretreatment mitigates doxorubicin-induced cardiac abnormalities in rats.
Why the study?
The study was conducted to investigate the potential cardioprotective effects of paricalcitol and vitamin D3 on doxorubicin cardiotoxicity using scintigraphic, electrocardiographic, and biochemical methods.
Does paricalcitol or vitamin D3 prevent doxorubicin-induced cardiotoxicity in a rat model?
Does paricalcitol or vitamin D3 prevent doxorubicin-induced cardiotoxicity in a rat model?
Paricalcitol and vitamin D3 demonstrate cardioprotective effects against doxorubicin-induced cardiotoxicity in a rat model through anti-inflammatory and antioxidant mechanisms.
Answers are grounded in this paper and cite their sources.
Supports preclinical testing of vitamin D analogs; leaves open translation to human doxorubicin cardiotoxicity.
AIM: We aimed to investigate the possible cardioprotective effects of paricalcitol (PR), its vitamin D receptor agonist, and vitamin D3 (VIT-D3) on an experimental model of doxorubicin (DX) cardiotoxicity by 99mTc-PYP scintigraphy, electrocardiographic (ECG) and biochemical methods. METHOD: Forty-two male Wistar/Albino rats (250‒300 g; aged 10‒12 weeks) were randomly separated into six groups, namely into control (CN), doxorubicin (DX), paricalcitol (PR), vitamin D3 (VIT-D3), paricalcitol + doxorubicin (PR+DX), and vitamin D3 + doxorubicin (VIT-D3+DX) groups. Cardiotoxicity was induced by three doses of DX (18 mg/kg, i.p.) at 24-hour intervals on days 18, 19 and 20. PR (0.5 ug/ kg, i.p) and VIT-D3 (5,000 IU/kg, i.p) were injected for 20 days before and after the application of DX (18 mg/kg, i.p.). On day 21 of the experiment, biochemical parameters [tumor necrosis factor TNF-alpha (TNF-α); interleukin-6 (IL-6), nitric oxide (NO), and cardiac troponin T (cTnT)], as well as ECG and scintigraphic (99mTc-PYP) features were assessed. RESULTS: Compared to CN, DX significantly raised TNF-α, IL-6, and NO in heart tissue, cTnT in serum, 99mTc-PYP uptake in the myocardium, and ECG parameters, specifically QRS complex duration, QT interval duration, and ST-segment amplitude, while also reducing heart rate (p<0.001). Pretreatment with PR and VIT-D3 mitigated these abnormalities produced by DX in the heart (p<0.001). CONCLUSION: Results show that vitamin D receptor agonist paricalcitol and vitamin D protect against DX-induced cardiotoxicity through anti-inflammatory and antioxidant effects (Fig. 4, Ref. 59). Text in PDF www.elis.sk Keywords: paricalcitol, doxorubicin, vitamin D, ECG, 99mTc-PYP scintigraphy, cardiotoxicity, inflammation.
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Köroğlu et al. (2024) studied Doxorubicin-induced acute cardiotoxicity (n=42). Paricalcitol and Vitamin D3 vs. Doxorubicin alone and healthy controls was evaluated on Biochemical parameters (TNF-α, IL-6, NO, cTnT), ECG, and scintigraphic features (p=<0.001). Pretreatment with paricalcitol and vitamin D3 significantly mitigated doxorubicin-induced electrocardiographic, biochemical, and scintigraphic abnormalities in rats.
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