Key result
Treatment with gallic acid (60 mg/kg and 120 mg/kg) attenuated cyclophosphamide-induced cardiotoxic and nephrotoxic effects in rats by restoring antioxidant defenses (p<0.05).
Why the study?
Does gallic acid prevent cyclophosphamide-induced cardiorenal dysfunction in a rat model?
Does gallic acid prevent cyclophosphamide-induced cardiorenal dysfunction in a rat model?
p-value: p=<0.05
Gallic acid demonstrates protective effects against cyclophosphamide-induced cardiorenal toxicity in a rat model through antioxidant and anti-inflammatory mechanisms.
Gallic acid merits further preclinical study in chemotherapy models; leaves open clinical translation and should not change practice.
Background Cardiac toxicity is one of the life-threatening complications of cancer therapy. Cyclophosphamide (CYP) is an alkylating agent with potent antineoplastic and immunosuppressive properties and possibly the most widely used antineoplastic agent. Chronic cardiotoxicity associated with CYP is characterized by progressive heart failure developing from weeks to years after therapy. Methods In this study, rats were administered with (60 mg/kg and 120 mg/kg) alone or in combination with single intraperitoneal (200 mg/kg) administration of CYP for 7 days. CYP was only administered on day 1. Results The administration of CYP led to a significant (p<0.05) increase in cardiac and renal malondialdehyde (MDA) contents and hydrogen peroxide (H2O2) generation. Also, the activities of catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) levels were significantly (p<0.05) reduced following CYP treatment. A significant (p<0.05) increase in serum myeloperoxidase (MPO) activity was recorded in rats administered CYP only. Electrocardiogram (ECG) showed a significant (p<0.05) increase in heart rate (HR) accompanied by transient decrease in QRS duration. Histologic examination revealed architectural anarchy of both heart and kidney of rats that received only CYP. Conclusions In this study, treatment with gallic acid (60 mg/kg and 120 mg/kg) restored the enzymic and non-enzymic antioxidants and also attenuated cardiotoxic and nephrotoxic effect of CYP through free radical scavenging activity, anti-inflammatory and improvement of antioxidant defence system.
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Ogunsanwo et al. (2017) studied Cyclophosphamide-induced cardiorenal dysfunction. Gallic acid vs. Cyclophosphamide only was evaluated on Cardiac and renal oxidative stress markers, antioxidant enzyme activities, and ECG changes (p=<0.05). Treatment with gallic acid (60 mg/kg and 120 mg/kg) attenuated cyclophosphamide-induced cardiotoxic and nephrotoxic effects in rats by restoring antioxidant defenses (p<0.05).
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