Cyclophosphamide (CP) is a common chemotherapeutic drug; however, it does have several toxic side effects, including cardiotoxicity. Beta (β)-glucan is a free radical scavenger and powerful antioxidative molecule. The effects of β-glucan on CP-induced cardiotoxicity were investigated in this experimental study. Twenty-eight Wistar albino rats were divided into the following four equal groups: control (no treatment), CP (200 mg/kg CP, intraperitoneally on day 2), β-glucan (50 mg/kg β-glucan, oral gavage for seven days), and CP+β-glucan (200 mg/kg CP, intraperitoneally on day 2+50 mg/kg β-glucan, oral gavage for seven days) groups. Histopathology, irisin, and caspase-3 expressions were evaluated in ventricular myocardial tissues. The CP group exhibited considerably more severe cardiac damage than the control group, according to histological evaluation. Immunohistochemically irisin expression was decreased, and caspase-3 expression was much higher in the CP group. β-glucan, on the other hand, improved histopathological changes and exhibited a protective potential against CP-induced cardiac tissue damage when combined with the CP group. Our findings showed that β-glucan could act as an effective cardioprotective molecule against the toxic effects caused by CP.
Key words: Cyclophosphamide, cardiotoxicity, β-glucan, irisin, caspase-3
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