Abstract
With population growth and aging, more and more patients with cerebral infarction have varying degrees of disability. ATP-sensitive potassium (KATP) channels regulate many cellular functions by coupling metabolic status with cell membrane electrical activity. Nicorandil (N-(2-hydroxyethyl)-nicotinamide nitrate) is the first KATP channel opener approved for clinical use. It has been reported that it might exert protective effects on the cerebral infarction by increasing cerebral blood flow and reducing inflammation. However, only a few studies explored its role in synaptogenesis. We made the rat model of middle cerebral artery occlusion (MCAO). Nicorandil was administered to rats via oral administration immediately after the surgery at a dose of 7.5 mg/kg and then daily for the next days. Infarct volume, cerebral edema, neurological deficits, cognitive impairment, and the level of Synaptophysin (SYP)、Growth associated protein-43 (GAP43) and neuronal nuclear antigen (NeuN) levels were measured to evaluate the effect of nicorandil. Our data showed that nicorandil treatment could decrease brain damage, improve learning and memory, and increase SYP、GAP43 and NeuN level. Taken together, we propose that nicorandil, as an opener of the KATP channel, provides a neuroprotective role in MCAO by promoting synaptic connections.
Highlights
Ischemic stroke is one of the leading causes of death worldwide and is characterized by high morbidity, mortality and disability rates
We investigated whether nicorandil could promote synaptogenesis in a rat middle cerebral artery occlusion (MCAO) model
The cerebral blood flow decreased to about 20% of the baseline level before the MCAO operation (Fig 1B)
Summary
Ischemic stroke is one of the leading causes of death worldwide and is characterized by high morbidity, mortality and disability rates. It places a heavy burden and suffering on society and family [1]. KATP channels are widely distributed in various tissues, including neurons, skeletal muscle, smooth muscle and pancreatic islet beta cells. Activation of KATP channels hyperpolarizes neurons, prevents excitotoxicity, stabilizes the membrane potential and reduces the ionic imbalance. It prevents neuronal damage and neurodegeneration caused by anoxic membrane
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