Aloin alleviates doxorubicin-induced cardiotoxicity in rats by abrogating oxidative stress and pro-inflammatory cytokines.

PURPOSE: Aloin, an anthraquinone present in the aloe species, possesses antiangiogenic, chemopreventive and antioxidant properties. It exerts cytotoxicity against breast cancer and ovarian cancer cell lines. These properties of aloin project it as a chemopreventive adjuvant to anticancer chemotherapy. METHODS: We evaluated the effect of concurrent oral administration of aloin against doxorubicin (DOX)-induced cardiotoxicity in rats. The protective effects of aloin against DOX-induced toxicity were evident as a statistically significant inhibition of a rise in the biochemical markers of myocardial damage including lactate dehydrogenase (LDH), creatinine kinase-myocardial band (CK-MB), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). RESULTS: Aloin dose dependently inhibited the DOX-induced changes in ECG like increased ST-height and prolonged QT interval. It protected heart against the lipid peroxidation and restored the levels of antioxidative defenses: reduced glutathione, catalase and superoxide dismutase. Aloin prominently reduced the levels of proinflammatory cytokines- TNF-α, IL-1ß and IL-6. Notably, the significant protective effects of aloin were evident even at the strikingly lower doses of 1 and 5 mg/kg per day. CONCLUSION: Our results highlight the necessity to further investigate the chemopreventive effects of aloin against other chemotherapeutic agents.

Aloin protects against arsenic trioxide-induced myocardial membrane damage and release of inflammatory cytokines.

Aloin exerts concentration-dependent pro-oxidant and antioxidant effects when tested in vitro. Such duality of effects has not been investigated through in vivo studies on aloin. We evaluated the effects of aloin at doses ranging between 1 and 125 mg/kg against the arsenic trioxide (As2O3)-induced cardiotoxicity in mice. As2O3 (5 mg/kg/day) was intraperitoneally administrated for 10 days. Aloin was administered through oral gavage at 1, 5, 25, and 125 mg/kg/day. As2O3 induced rise in ST height and QT interval in ECG, increased oxidative stress, and depleted the antioxidative defense. As2O3 increased inflammatory cytokine concentrations in the heart. Aloin dose dependently inhibited the As2O3-induced cardiotoxicity. There was no evidence of increased oxidative stress in the low-dose aloin-treated mice receiving As2O3. Our results indicate that aloin possesses cardioprotective potentials and its pro-oxidant effect is not evident in vivo at tested doses.