Neuroprotective effects of potassium channel openers on cerebral ischemia-reperfusion injury in diabetic rats

• Main Authors: Anand B. Pithadia (Author), Shital S. Panchal (Author), Denvanshu J. Patel (Author)
• Format: Book
• Published: Faculty of Pharmacy, Cairo University, 2017-06-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Objectives: 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). Methods: Potassium channel openers - cromakalim, cinnarizine and nicorandil; potassium channel blocker -glibenclamide, insulin (as an antidiabetic standard), telmisartan (as an anti-hypertensive standard agent) and vitamin E (as an antioxidant and antiapoptotic standard agent) were given for 3 days in streptozotocin (45 mg/kg i.v.) induced type I diabetic rats along with middle cerebral artery occlusion. After 24 h of surgery, plasma glucose, neurobehavioral score, cerebral infarct volume, blood pressure and caspase-3 levels were measured to evaluate the mechanism of potassium channel openers (KCOs) for neuroprotection. Results: Following STZ administration and ischemia-reperfusion, blood sugar, neurobehavioral score, cerebral infarct volume and caspase-3 levels were significantly high in diabetic-IR groups. Treatment with cromakalim, cinnarizine, nicorandil, insulin and vitamin E significantly reduce neurobehavioral score while nicorandil and vitamin E significantly reduced cerebral infarct volume. Caspase-3 levels were significantly reduced by cromakalim and nicorandil treated animals. Except insulin and glibenclamide, none of the agents significantly reduce plasma glucose levels. Conclusion: Treatment of ischemic stroke with potassium channel openers in T1DR is neuroprotective. Inhibition of apoptosis may contribute to their neuroprotective effects after stroke in T1DR.

Item Description

1110-0931
10.1016/j.bfopcu.2016.09.002