Key result
Geraniol reduces cardiac injury, inflammation, and apoptosis in mice with cyclophosphamide-induced cardiotoxicity.
Why the study?
The study was conducted to explore the effect of geraniol on cyclophosphamide-induced cardiotoxicity.
Does geraniol alleviate cyclophosphamide-induced cardiotoxicity in mice?
Does geraniol alleviate cyclophosphamide-induced cardiotoxicity in mice?
Geraniol attenuates cyclophosphamide-induced cardiotoxicity in mice through antioxidant, anti-inflammatory, and antiapoptotic mechanisms.
Does not support clinical use of geraniol; hypothesis-generating in animal models of cyclophosphamide cardiotoxicity.
Objective: To explore the effect of geraniol on cyclophosphamide- induced cardiotoxicity. Methods: Mice were divided into five groups: the control group, the cyclophosphamide group (200 mg/kg cyclophosphamide, i.p. on day 7), the group treated with geraniol 100 and 200 mg/kg from day 1 to day 14, along with a single dose of cyclophosphamide on day 7, and the geraniol alone group (200 mg/kg geraniol from day 1 to day 14). At the end of the study, animals were sacrificed, and blood and heart were collected and analyzed for biochemical, histopathological, and immunohistochemical changes. Results: Treatment with 200 mg/kg geraniol significantly reduced the levels of cardiac injury markers, malondialdehyde, and inflammatory and apoptotic markers, while increasing antioxidant activities in mice with cyclophosphamide-induced cardiotoxicity. Moreover, it remarkably alleviated histopathological aberrations in cardiac tissue. Conclusions: Geraniol attenuates cyclophosphamide-induced cardiotoxicity via antioxidant, anti-inflammatory, and antiapoptotic effects.
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Karim et al. (2024) studied Cyclophosphamide-induced cardiotoxicity. Geraniol vs. Cyclophosphamide alone was evaluated on Cardiac injury markers, malondialdehyde, inflammatory and apoptotic markers, antioxidant activities, and histopathological aberrations. Geraniol at 200 mg/kg significantly reduced cardiac injury markers, inflammation, and apoptosis, while increasing antioxidant activities in mice with cyclophosphamide-induced cardiotoxicity.
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