دورية أكاديمية

The specific VPAC2 agonist Bay 55-9837 increases neuronal damage and hemorrhagic transformation after stroke in type 2 diabetic rats.

التفاصيل البيبلوغرافية
العنوان: The specific VPAC2 agonist Bay 55-9837 increases neuronal damage and hemorrhagic transformation after stroke in type 2 diabetic rats.
المؤلفون: Darsalia, Vladimer, Mansouri, Shiva, Wolbert, Petra, Barde, Swapnali, Sjöholm, Åke, Patrone, Cesare
المصدر: Neuropeptides; Apr2013, Vol. 47 Issue 2, p133-137, 5p
مصطلحات موضوعية: NEURONS, BRAIN damage, STROKE, LABORATORY rats, TYPE 2 diabetes treatment, PHARMACODYNAMICS, DEATH rate, HYPOGLYCEMIC agents
مستخلص: Abstract: VPAC2 receptor is a potential target for the treatment of type 2 diabetes and may also convey neuroprotective effects. The aim of this study was to determine the potential efficacy of the VPAC2 receptor agonist Bay 55-9837 against stroke in type-2 diabetic Goto-Kakizaki (GK) rats. GK rats were treated intravenously once daily for 7days with 0.25 or 0.025nmol/kg Bay 55–9837 or vehicle before inducing stroke by transient middle cerebral artery occlusion. Treatments were then continued for 7 further days. The glycemic effects of Bay 55-9837 were assessed by measuring fasting blood glucose and oral glucose tolerance. The severity of stroke was measured by assessing ischemic volume. The results show that Bay 55-9837 is not effective in lowering fasting glycemia and does not facilitate glucose disposal. The highest dose of Bay 55-9837 (0.25nmol/kg) led to increased mortality and brain hemorrhage when compared to control. The lower dose of Bay 55-9837 (0.025nmol/kg) did not increase mortality rate but caused a threefold increase of the ischemic lesion size with signs of brain hemorrhages as compared to control. In conclusion, Bay 55-9837 did not show antidiabetic or antistroke efficacy in the type 2 diabetic GK rat. Contrarily, Bay 55-9837 treatment led to increased mortality and worsening of the severity of stroke. [Copyright &y& Elsevier]
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قاعدة البيانات: Supplemental Index
الوصف
تدمد:01434179
DOI:10.1016/j.npep.2012.08.008