Abstract
BackgroundThe functions of free radicals on the effects of insulin that result in protection against cerebral ischemic insult in diabetes remain undefined. This present study aims to explain the contradiction among nitric oxide (NO)/superoxide/peroxynitrite of insulin in amelioration of focal cerebral ischemia–reperfusion (FC I/R) injury in streptozotocin (STZ)-diabetic rats and to delineate the underlying mechanisms. Long-Evans male rats were divided into three groups (age-matched controls, diabetic, and diabetic treated with insulin) with or without being subjected to FC I/R injury.ResultsHyperglycemia exacerbated microvascular functions, increased cerebral NO production, and aggravated FC I/R-induced cerebral infarction and neurological deficits. Parallel with hypoglycemic effects, insulin improved microvascular functions and attenuated FC I/R injury in STZ-diabetic rats. Diabetes decreased the efficacy of NO and superoxide production, but NO and superoxide easily formed peroxynitrite in diabetic rats after FC I/R injury. Insulin treatment significantly rescued the phenomenon.ConclusionsThese results suggest that insulin renders diabetic rats resistant to acute ischemic stroke by arresting NO reaction with superoxide to form peroxynitrite.
Highlights
The functions of free radicals on the effects of insulin that result in protection against cerebral ischemic insult in diabetes remain undefined
General characteristics in Non-diabetic control, STZ-diabetic, and insulin-treated diabetic rats Animals treated with STZ resulted in consistent hyperglycemia and hypoinsulinemia that persisted over the three-week period
(4) Diabetes increased nitric oxide (NO) reaction with superoxide to form peroxinitrite in the cerebrum after focal cerebral ischemia–reperfusion (FC I/R) injury, and this effect was reversed by insulin treatment
Summary
The functions of free radicals on the effects of insulin that result in protection against cerebral ischemic insult in diabetes remain undefined. This present study aims to explain the contradiction among nitric oxide (NO)/superoxide/peroxynitrite of insulin in amelioration of focal cerebral ischemia–reperfusion (FC I/R) injury in streptozotocin (STZ)-diabetic rats and to delineate the underlying mechanisms. The roles of free radicals on the effects of insulin that result in protection against cerebral ischemic insult in diabetes remain undefined. The secondary aim is to explore the possible mechanisms (with specific focus on NO/superoxide/peroxynitrite) of insulin in amelioration of focal cerebral ischemia-reperfusion (FC I/R) injury in streptozotocin (STZ)-diabetic rats
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