Objective:To investigate the effect and mechanism of palmatine on diabetic mouse aorta. Methods:Totally 32 db/db mice（8 weeks old）were randomly divided into diabetic model group

low-dose palmatine group[75 mg/（kg·d）]

medium-dose group[150 mg/（kg·d）] and high-dose group[300 mg/（kg·d）]. Eight db/m mice were used as control group. The palmatine was administered by oral gavage for 12 weeks. The diabetic model group and control group mice were given the same volume of saline. Then

HE staining was used to determine the pathological changes of the thoracic aorta tissues. Electron microscope was used to observe the ultrastructural changes of the thoracic aorta tissues. The fasting blood glucose（FBG） and lipids（total cholesterol

TC;triglyceride

TG） were analyzed by an automatic biochemical analyzer. The serum total antioxidant capacity（T-AOC）

malondialdehyde（MDA）

reactive oxygen species（ROS）and superoxide dismutase（SOD）were measured by commercial ELISA kit. Western blot was used to determine the expression of the nuclear factor E2-related factor 2（Nrf2）and heme oxygenase-1（HO-1）protein in the thoracic aorta. Results:HE staining results indicated that the thoracic aorta lesions were significantly reduced in the groups after palmatine treatment. Electron microscope results indicated that the thoracic aorta damage under ultrastructural observation was also significantly reduced in the groups after palmatine treatment. Compared with those of diabetic model group

the levels of blood FBG and lipids were significantly repressed

and the levels of serum MDA and ROS were significantly decreased

but the activity of serum SOD and T-AOC was significantly increased. Western blot results showed that Nrf2 and HO-1 protein expressions were significantly increased in the groups after palmatine treatment. Meanwhile

there were significantly differences among palmatinedose groups（P =0.000

P =0.000

P =0.000

P=0.000

P=0.000

P=0.000

P=0.000

P=0.000）. Conclusion:Palmatine effectively protects diabetic mouse aorta tissues

which may be achieved by decreasing blood FBG and lipids

inducing Nrf2/HO-1 signaling and repressing oxidative stress.