Abstract
Ketamine, a phencyclidine derivative, is most usually used to induce dissociative general anesthesia, but it is also beneficial for bronchospasm, a congenital cardiac disease with the right to left shunting, and, more recently, treatment of resistant depression. Several studies have revealed that ketamine may help damaged neurons recover. Ketamine has been proven to offer neuroprotection in a variety of neuro injury models. Following that, many routes and targets were identified to demonstrate how ketamine may protect the brain. Ketamine has been shown to modulate neuronal excitotoxicity, apoptosis, and inflammation, among other things. The present work examined the relative interaction of ketamine with potential targets of brain excitotoxicity, apoptosis, and inflammation using an in-silico approach. Furthermore, ketamine has been shown to protect against isoflurane-induced cognitive impairment in rats.
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