Oral supplementation of catalpol ameliorates diabetic encephalopathy in rats.
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.
Wang
Cheng-Fang
CF
The First Affiliated Hospital, Dalian Medical University, Dalian, Liaoning 116023, PR China.
Li
Dan-Qing
DQ
Xue
Hong-Yu
HY
Hu
Bo
B
D000284:Administration, Oral; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000178:diet therapy* / Q000503:physiopathology; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005960:Glucosides / Q000008:administration & dosage*; D005979:Glutathione Peroxidase / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D057888:Iridoid Glucosides; D039823:Iridoids / Q000008:administration & dosage*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000187:drug effects; D020932:Nerve Growth Factor / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors
D001786:Blood Glucose; D005960:Glucosides; D057888:Iridoid Glucosides; D039823:Iridoids; C078040:catalpol; D008315:Malondialdehyde; D020932:Nerve Growth Factor; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase