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Ferulic acid ameliorates doxorubicin-induced cardiac toxicity in rats

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Abstract

Ferulic acid (FA) is a phenolic compound with potent antioxidant activity. The objective of the study was to study the protective effects of FA on doxorubicin (Dox)-induced myocardial toxicity in rats. Wistar rats received vehicle (control) or Dox (20 mg/kg, i.p.) or telmisartan (Tel; 10 mg/kg, p.o.) or ferulic acid (20 mg/kg and 40 mg/kg, p.o.) for 7 days followed by treatment with Dox (20) on the fifth day of treatment, except the control group. On day 8, electrocardiographic parameters were recorded followed by blood withdrawal and then the animals were sacrificed for histopathology. Administration of Dox showed prolonged RR, QTc interval, and QRS complex. The levels of serum CK-MB, LDH, IL-1β, and IL-6 were significantly increased (p < 0.01). Similarly, levels of Ca+2, Mg+2 ATPase, and Ca+2 ATPase and expression of ANP and BNP were significantly higher as compared to the control. In the FA-treated group, ECG was normal. The serum levels of CK-MB, LDH, IL-1β, and IL-6 were not elevated. Heart tissue Ca+2, Mg+2 ATPase, and Ca+2 ATPase did not show a statistical difference compared to the control group. The FA treatment attenuated the expression of ANP and BNP. FA (20 and 40) augmented myocardial GSH and Na+/K+ ATPase. Histopathology of the heart confirmed the cardioprotective effect of FA.

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Acknowledgements

The authors would like to acknowledge Prof. M. N. Navale, Founder, STES, and Dr. K. G. Bothara, Principal, SIOP, for providing the necessary facilities to carry out the research work.

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Correspondence to Urmila Aswar.

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The experimental protocol was approved by the Institutional Animal Ethical Committee (IAEC) of SIOP, Pune, constituted as per the Committee for Purpose of Supervision and Control on the experimental animal CPCSEA reg. no 1139/a/07/ CPCSEA (Protocol approval no. SIOP/IAEC/2012/21B).

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Aswar, U., Mahajan, U., Kandhare, A. et al. Ferulic acid ameliorates doxorubicin-induced cardiac toxicity in rats. Naunyn-Schmiedeberg's Arch Pharmacol 392, 659–668 (2019). https://doi.org/10.1007/s00210-019-01623-4

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  • DOI: https://doi.org/10.1007/s00210-019-01623-4

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