Abstract
Scutellarin, which is extracted from the dried plant ofErigeron breviscapus, has been reported to protect the neural injury against excitotoxicity induced by ischemia. However, there are a few studies on the protective effects of scutellarein, which is the main metabolite of scutellarin in vivo. Thus, this study investigated the neuroprotective effects of scutellarein on cerebral ischemia/reperfusion in rats by bilateral common carotid artery occlusion (BCCAO) model, through the analysis of endogenous amino acids using HILIC-MS/MS, and evaluation of Ca2+concentration together with Ca2+-ATPase activity. The results showed that scutellarein having good protective effects on cerebral ischemia/reperfusion might by decreasing the excitatory amino acids, increasing the inhibitory amino acids, lowing intracellular Ca2+level, and improving Ca2+-ATPase activity, which suggested that scutellarein might be a promising potent agent for the therapy of ischemic cerebrovascular disease.
Highlights
Ischemic cerebrovascular disease is the main cause of disability and death among the elderly people [1]
The depolarization is mediated by the metabolic failure which is caused by ischemia, and the results indicate that there is an influx of Ca2+ via voltagesensitive Ca2+ channels, initiate a flood of amino acid neurotransmitters, especially glutamate and aspartic acid [3], release into the synaptic cleft
The Ca2+-ATPase activity in the scutellarein pretreated group increased in a dose-dependent manner. These results indicated that the protective effect of scutellarein might be due to its cerebral neuroprotection by inhibiting Ca2+ overload and enhancing Ca2+-ATPase activity
Summary
Ischemic cerebrovascular disease is the main cause of disability and death among the elderly people [1]. The increasing evidences showed that the excessive release of various amino acid neurotransmitters is one pathogenesis during ischemia reperfusion [2], indicating that the amino acid levels could be diagnostic markers. The depolarization is mediated by the metabolic failure which is caused by ischemia, and the results indicate that there is an influx of Ca2+ via voltagesensitive Ca2+ channels, initiate a flood of amino acid neurotransmitters, especially glutamate and aspartic acid [3], release into the synaptic cleft. The excitatory amino acids, which are the most important amino acid neurotransmitters, could induce a cascade of events leading to cell death [4, 5]. The determination of these amino acid neurotransmitters is very important to evaluate the global cerebral ischemic injury
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