2024, Vol. 28 ›› Issue (2): 237-241

Establishment and evaluation of a streptozotocin-induced diabetic encephalopathy rat model

Chen Simin1, 2, Hu Yingjun1, Yan Wenrui1, Ji Le1, Shao Mengli1, Sun Ze1, 3, Zheng Hongxing1, 4, Qi Shanshan1, 2   

Abstract: BACKGROUND: Animal models of diabetic encephalopathy that have been studied mainly include streptozotocin-induced model, high-sugar and high-fat diet-induced model and spontaneous animal model. Establishing a simple, easy, short-cycle, safe and effective model of diabetic encephalopathy can help to explore the subsequent pathogenesis and screen therapeutic drugs.
OBJECTIVE: To further explore and evaluate the method of building diabetic encephalopathy rat models.
METHODS: Twenty Sprague-Dawley rats were randomly divided into control (n=10) and model (n=10) groups. Rats in the model group were given a single injection of 45 mg/kg streptozotocin in the left lower abdominal cavity, and those in the control group were given the same amount of citrate buffer. During the experiment, the body mass, feed intake, water intake and blood glucose were measured. After 8 weeks, the glucose tolerance and oxidative stress levels were measured, and the pathological changes of brain tissue and the expression of apoptotic proteins were compared between groups.
RESULTS AND CONCLUSION: Compared with the control group, the food intake, water intake, encephalization quotient, blood glucose and area under the blood glucose curve were significantly increased in the model group, while the body mass decreased significantly (P < 0.01). Histopathological examination of the brain showed that compared with the control group, the number of surviving nerve cells was significantly reduced in the model group (P < 0.01), with more significant pathological damage of nerve cells. Compared with the control group, the activities of serum superoxide dismutase, catalase and glutathione in the model group were significantly decreased (P < 0.01), and the content of oxidative malondialdehyde was significantly increased (P < 0.05). The expression levels of apoptosis-related proteins Bax and Caspase-3 in brain tissue increased in the model group compared with the control group, while the expression of Bcl-2 decreased (P < 0.01). In conclusion, an 8-week injection of 45 mg/kg streptozotocin can cause obvious pathological damage to the brain tissue of diabetic rats, to successfully establish the rat model of diabetic encephalopathy.

Key words: diabetic encephalopathy, streptozotocin, animal model, brain tissue, rat, high blood glucose, oxidative stress, neuronal cell apoptosis