Subchronic Exposure of Apigenin Induces Hepatic Oxidative Stress in Male Rats

Abstract

Apigenin (4’, 5, 7-trihydroxyflavone, AP), a dietary flavonoid, is reported to have several therapeutic effects in different diseases including cancer. In the present study, in order to explore the potential mechanism and provide the references for further studies, we investigated the effect of apigenin at various dosages on the hepatic oxidative stress of male rats. Totally 48 SD male rats were randomly divided into control group (saline, 1 ml/100g·bw), low-dose group (AP, 234 mg/kg·bw), middle-dose group (AP, 468 mg/kg·bw) and high-dose group (AP, 936 mg/kg·bw). The rats were administered with apigenin or saline via intragastriation once a day, 6 days per week, and 5 consecutive weeks. Rats were sacrificed and the livers were harvested and then immediately preserved at ﹣20°C. Liver homogenate was prepared before detection. Hepatic malondialdehyde (MDA), nitric oxide syntheses (NOS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC) and glutathione (GSH) were determined by colorimetric methods according to the provided procedures. The weights of liver and spleen in apigenin treatment groups did not reveal statistically significant difference when compared with that in the control group (P > 0.05). Total protein (TP), albumin (ALB) and globulin (GLO) in apigenin treatment groups were significantly lower than those in the control group (P < 0.05). SOD in the middle-dose group (AP, 468 mg/kg·bw) and high-dose group (AP, 936 mg/kg·bw) were significantly higher than that in the control group (P < 0.05). T-AOC, CAT and GSH-Px in apigenin treatment groups were significantly lower than those in the control group (P < 0.05). In high-dose AP group (AP, 936 mg/kg·bw), apigenin can result in the reduction of T-AOC, thus leading to the oxidative damage of liver tissues. In contrast, in middle-dose AP group (AP, 468 mg/kg·bw), apegenin can reduce the elimination capacity of oxygen free radicals.