Research code: 1400-3-105-22066
Ethics code: IR.IUMS.FMD.REC.1400.588
Clinical trials code: no
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. , azizi.y@iums.ac.ir
Abstract: (571 Views)
Introduction: Doxorubicin is used in the treatment of various types of malignancies including lymphoma, leukemia and breast cancer. Although cardiac toxicity is the main side effect of this drug, liver and lung toxicity have also been reported. Apigenin is a flavonoid with antioxidant, anti-inflammatory, and anti-tumor properties. The aim of this study was to investigate the effects of apigenin on liver and lung toxicity caused by doxorubicin and the possible role of nitric oxide.
Materials and methods: 60 male Wistar rats were randomly divided into 6 groups (n=10). For induction of liver and lung toxicity in groups 3, 4, 5, and 6, doxorubicin was injected intraperitoneally (i.p.) in 6 doses of 2 mg/kg every 48 hours. Apigenin was administered orally with a dose of 50 mg/kg in groups 2, 4, and 6. To prevent the formation of nitric oxide (NO), L-NAME was injected i.p. in groups 5 and 6 at 6 doses of 30 mg/kg every 48 hours.
Findings: Apigenin could prevent tissue changes caused by doxorubicin in lung and liver. It also improved weight loss and reduced fibrosis in the lung (p<0.05). Doxorubicin injection and apigenin treatment did not cause significant changes in liver enzymes and liver fibrosis. Inhibition of NO by L-NAME prevented almost all protective effects of apigenin.
Conclusion: Apigenin reduced the damages induced by doxorubicin. It seems that inhibition of nitric oxide decreases the protective effects of apigenin. Apigenin probably exerts its protective effects in liver and lung toxicity caused by doxorubicin by increasing the expression of NO.