Key result
Chlorogenic acid reduces doxorubicin-induced troponin T elevation by ~45% in rats.
Why the study?
Clinical application of doxorubicin is limited by cardiotoxicity, and the in vivo cardioprotective properties and mechanisms of chlorogenic acid remained to be evaluated.
Does oral chlorogenic acid pretreatment attenuate myocardial injury, oxidative stress, and apoptosis in a rat model of acute doxorubicin-induced cardiotoxicity?
Does oral chlorogenic acid pretreatment attenuate myocardial injury, oxidative stress, and apoptosis in a rat model of acute doxorubicin-induced cardiotoxicity?
Preclinical evidence in rats demonstrates that chlorogenic acid protects against acute doxorubicin-induced cardiotoxicity by activating the Nrf2/HO-1 antioxidant pathway and suppressing dityrosine and caspase-3 expression.
Answers are grounded in this paper and cite their sources.
Should not change doxorubicin management; leaves open whether chlorogenic acid cardioprotection translates to patients.
(1) Background: Doxorubicin (DOX) is extensively used for cancer treatments; however, its clinical application is limited because of its cardiotoxic adverse effects. A combination of DOX and agents with cardioprotective properties is an effective strategy to ameliorate DOX-related cardiotoxicity. Polyphenolic compounds are ideal for the investigation of novel cardioprotective agents. Chlorogenic acid (CGA), an essential dietary polyphenol found in plants, has been previously reported to exert antioxidant, cardioprotective, and antiapoptotic properties. The current research evaluated CGA's in vivo cardioprotective properties in DOX-induced cardiotoxicity and the probable mechanisms underlying this protection. (2) Methods: CGA's cardioprotective properties were investigated in rats that were treated with CGA (100 mg/kg, p.o.) for fourteen days. The experimental model of cardiotoxicity was induced with a single intraperitoneal (15 mg/kg i.p.) injection of DOX on the 10th day. (3) Results: Treatment with CGA significantly improved the DOX-caused altered cardiac damage markers (LDH, CK-MB, and cTn-T), and a marked improvement in cardiac histopathological features accompanied this. DOX downregulated the expression of Nrf2/HO-1 signaling pathways, and the CGA reversed this effect. Consistently, caspase-3, an apoptotic-related marker, and dityrosine expression were suppressed, while Nrf2 and HO-1 expressions were elevated in the cardiac tissues of DOX-treated rats after treatment with the CGA. Furthermore, the recovery was confirmed by the downregulation of 8-OHdG and dityrosine (DT) expressions in immunohistochemical findings. (4) Conclusions: CGA demonstrated a considerable cardioprotective effect against DOX-induced cardiotoxicity. One of the possible mechanisms for these protective properties was the upregulation of the Nrf2/HO-1-dependent pathway and the downregulation of DT, which may ameliorate oxidative stress and cardiomyocyte apoptosis. These findings suggest that CGA may be cardioprotective, particularly in patients receiving DOX-based chemotherapy.
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Çiçek et al. (2023) studied Doxorubicin-induced cardiotoxicity (n=28). Chlorogenic acid vs. Doxorubicin alone (15 mg/kg i.p. on day 10) and vehicle control (PBS daily for 14 days) was evaluated on Serum cardiac troponin T (cTn-T) concentration (ng/mL) (p=<0.0001). Chlorogenic acid pretreatment significantly attenuated doxorubicin-induced elevation of serum cTn-T (0.61 vs 1.10 ng/mL, p<0.0001) and other cardiac injury markers in rats.
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