Key result
Daidzein reduces cardiac injury and oxidative stress markers in 5-FU-induced cardiotoxicity in rats.
Why the study?
The study was conducted to determine the cardioprotective effect of daidzein against 5-fluorouracil-induced cardiotoxicity.
Does daidzein prevent 5-fluorouracil-induced cardiotoxicity in Wistar rats?
Does daidzein prevent 5-fluorouracil-induced cardiotoxicity in Wistar rats?
p-value: p=<0.01
Daidzein demonstrates potential cardioprotective effects against 5-fluorouracil-induced cardiotoxicity in a rat model by improving oxidative stress and cardiac injury biomarkers.
The aim of the study was to determine the cardioprotective effect of daidzein in 5-fluorouracil-induced cardiotoxicity. The animals of the standard group were treated with carvedilol 10 mg kg-1, and DDZ5 and DDZ10 groups were treated with daidzein for 8 days at doses of 5 mg kg-1 and 10 mg kg-1, respectively, with induction of disease on day 5 with 5-fluorouracil in all groups. The results were determined by evaluating biochemical parameters such as CK-MB, LDH, cTnl, GSH, MDA, MPO and total cholesterol, as well as histopathological study. It was found that both daidzein 5 mg kg-1 and daidzein 10 mg kg-1 considerably (p<0.01) decreased the animal's levels of MDA, MPO, LDH and CKMB compared to the negative control group. The level of GSH in DDZ5 and DDZ10 animals was significantly (p<0.01) higher than negative control animals. It can be concluded from this study that daidzein holds significant potential to prevent as well as manage the cardiotoxicity caused by 5-FU.
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Srivastava et al. (2025) studied 5-fluorouracil-induced cardiotoxicity. Daidzein vs. Negative control group and carvedilol 10 mg kg-1 was evaluated on Biochemical parameters (CK-MB, LDH, cTnl, GSH, MDA, MPO, total cholesterol) and histopathological study (p=<0.01). Daidzein at 5 mg/kg and 10 mg/kg significantly decreased levels of MDA, MPO, LDH, and CKMB (p<0.01) and increased GSH (p<0.01) compared to negative control in 5-FU-induced cardiotoxicity in rats.
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