A total of 25 mice were randomly divide into control group（given saline）， model group （given 120 mg·kg^－1 D-galactose）， positive control group （given 120 mg·kg^－1 D-galactose and 100 mg·kg^－1 VE）， low dose of BCP group（given 120 mg·kg^－1 D-galactose and 200 mg·kg^－1 BCP）， high dose of BCP group （given 120 mg·kg^－1 D-galactose and 400 mg·kg^－1 BCP）. The mice in control group were injected intraperitoneally daily with saline， and the mice in the other groups were injected with D-galactose intraperitoneally to construct the aging models. The body weights， liver indexes，and kidney indexes of the mice in various groups were detected；the serum activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） and the serum levels of malondialdehyde （MDA） of the mice in various groups were detected；HE staining was used to detect the morphology of liver tissue of the mice in various groups； Western blotting method was used to detect the expression levels of p53 and p16 proteins in kidney tissue of the mice in various groups.

After 7 weeks of continuous injection of D-galactose， compared with control group， the body weight of the mice in model group was significantly decreased （P<0.05）， and the liver index and kidney index were increased （P<0.05），the activities of SOD and GSH-Px in serum were decreased （P<0.01）， and the level of serum MDA was increased （P<0.01）； the expression levels of p53 and p16 proteins in kidney tissue were increased （P<0.01）； meanwhile， the hepatocyte edema was obvious， the liver tissue injury was severe. Compared with model group， the body weights of the mice in low and high doses of BCP groups were significantly increased （P<0.05），the liver indexes and kidney indexes were decreased （P<0.05）， the activities of SOD and GSH-Px in serum were increased （P<0.01）， the levels of serum MDA were decreased （P<0.01），and the expression levels of p53 and p16 proteins in kidney tissue were decreased （P<0.05 or P<0.01 ）； the morphology of liver cells was gradually normalized and the liver injury was alleviated.

BCP can inhibit the D-galactose-induced aging in the mice by inhibiting the oxidative stress and its downstream p53 and p16 signaling pathways.