alexa Neuroprotective Effect Of Potassium Channel Openers On Cerebral Ischemia-reperfusion Injury In Type I Diabetic Rats
ISSN: 2168-975X

Brain Disorders & Therapy
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3rd International Conference on Neurological Disorders and Brain Injury
April 18-19, 2017 London, UK

Anand B Pithadia, Shital J Panchal, B N Suhagia, Arun Soni and Tejal Soni
Dharmsinh Desai University, India
Nirma University, India
Posters & Accepted Abstracts: Brain Disord Ther
DOI: 10.4172/2168-975X-C1-015
Abstract
Cerebral ischemic stroke is an obstruction blood supplied to brain. It is of either ischemic stroke (IS) or hemorrhagic stroke. Diabetes mellitus increase risk for macro-vascular and micro-vascular complications. This study was done to estimate the potential neuroprotective role of potassium channel openers in cerebral ischemia-reperfusion (IR) injury in streptozotocin (STZ) induced type-I diabetic rats (T1DR). Potassium channel openers-cromakalim, cinnarizine and nicorandil; potassium channel blocker- glibenclamide, insulin (as an anti-diabetic standard), telmisartan (as an anti-hypertensive standard agent) and vitamin E (as an antioxidant and anti-apoptotic standard agent) were given for three days in streptozotocin (45 mg/kg) induced type I diabetic rats along with transient middle cerebral artery occlusion. After 24 hours of surgery, serum glucose, neurobehavioral score, cerebral infarct volume, post ischemic body weight changes, superoxide dismutase activity, nitrite levels and malondialdehyde (MDA) levels were measured to evaluate mechanism of potassium channel openers (KCOs) for neuroprotection. Following STZ administration and ischemia-reperfusion, blood sugar, neurobehavioral score, cerebral infarct volume, MDA and nitrite levels were significantly high and SOD activity was significantly less in diabetic–IR groups. Treatment with all three potassium channel openers showed neuroprotective activity in diabetic IR groups. These activities were more with cromakalim and nicorandil compared to cinnarizine. Except insulin and glibenclamide, none of the agent significantly reduces plasma glucose levels. Treatment of ischemic stroke with potassium channel openers in T1DR is neuroprotective. Inhibition of oxidative stress may contribute to their neuroprotective effects after stroke in T1DR.
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