Luteolin attenuates diabetes-associated cognitive decline in rats

Diabetes mellitus can cause dysfunction of the central nervous system called “diabetic encephalopathy”. Although various oral drugs are used to treat diabetes, they do not prevent the development of diabetes-associated cognitive decline in rats, and novel strategies for the prevention and treatment are urgently needed. Luteolin, a flavonoid isolated from Cirsium japonicum, has antioxidant, anti-inflammatory and neuroprotective activities. However, no report is available on influence of luteolin on streptozotocin-induced memory impairment. Therefore, we tested its influence against cognitive dysfunction in streptozotocin-induced diabetic rats using Morris water maze test. Nissl's staining, choline esterase (ChE) activity as marker of cholinergic function and oxidative stress were assessed in the cerebral cortex and hippocampus to evaluate the neuropathological changes and the effects of luteolin on diabetic rats. The results showed that streptozotocin-induced diabetes produced obvious neuron damage and cognitive dysfunction coupling with markedly increased oxidative stress and ChE activity in the brain. In contrast, chronic treatment with luteolin (50 and 100 mg/kg) improved neuronal injury and cognitive performance by attenuating oxidative stress and ChE activity in diabetic rats. In conclusion, the present study suggested that oral supplementation of luteolin might be a potential therapeutic strategy for the treatment and/or prevention of diabetic encephalopathy.

► STZ-induced diabetes can cause dysfunction of the central nervous system.
► MWM test showed that luteolin improved the learning and memory of diabetic rats.
► Treatment with luteolin improved neuronal injury in diabetes.
► Treatment with luteolin attenuated oxidative stress and ChE activity in diabetes.
► Luteolin might be a potentially effective therapy for diabetic encephalopathy.