Diabetes mellitus can cause dysfunction of the central nervous system called "
diabetic encephalopathy." Although
insulin and various oral drugs are used to treat diabetes, they do not completely prevent the development of
diabetic encephalopathy, and novel strategies for the prevention and treatment are urgently needed.
Catalpol, an
iridoid glycoside, has properties of anti-
inflammation,
antioxidant and decreasing
blood glucose level and thus has the possibility of treating
diabetic encephalopathy. Therefore, the study was designed to investigate the effects of
catalpol on
diabetic encephalopathy in rats. A single dose of 65 mg/kg
streptozotocin was injected intraperitoneally to induce diabetes. Intragastric infusion of
catalpol was performed for 6 weeks with the doses of 10, 50 and 100 mg/kg, respectively. The Y-type maze test, biochemical measurement, Nissl staining and the
terminal deoxynucleotidyl transferase-mediated
UTP nick end labeling methods were used to evaluate the neuropathological changes and the effects of
catalpol on diabetic rats. The results showed that
streptozotocin-induced diabetes produced obvious neuron damage and
cognitive dysfunction coupling with markedly increased oxidative stress in the brain. Long-term oral supplementation of
catalpol improved neuronal injury and
cognitive dysfunction by attenuating oxidative stress. The effects that
catalpol could both increase the
nerve growth factor concentration and decrease the
blood glucose level were related with the function of defending against oxidative stress of
catalpol. The study suggested that oral supplementation of
catalpol might be a potential therapeutic strategy for the treatment and/or prevention of
diabetic encephalopathy.