Abstract
Sesamin, a major lignan found in sesame oil, is widely used in traditional Chinese medicine for its bioactivities. However, the information on the neuroprotective effects of sesamin against ischemia- or glutamate-induced excitotoxic injury is limited. This study aimed to investigate the neuroprotective effects of sesamin against focal cerebral ischemia in vivo and N-methyl-d-aspartate (NMDA)-induced neurotoxicity in vitro. Sesamin (43.2 mg/kg) attenuated cerebral ischemic injury in mice induced by 2 h of middle cerebral artery occlusion and reperfusion. Furthermore, treatment with 0.1 μM sesamin significantly decreased the number of apoptotic neuronal cells in cultured neurons after exposure to 200 μM NMDA. Western blot and calcium imaging results indicated that sesamin protected neurons against excitotoxicity by restoring the balance of apoptotic proteins and inhibiting calcium overload in cultured neurons after exposure to NMDA. Our findings provide a new insight into the development of natural anti-excitotoxicity agents.
Highlights
Glutamate is the major excitatory neurotransmitter in the central nervous system (CNS) [1]
The neuroprotective effect of sesamin against ischemiareperfusion injury was evaluated via neurological scoring, infarct size measurement, and Nissl staining
Sesamin has been reported to rescue neuronal PC12 cells from apoptosis and death induced by the MPP+ activation of microglia cells [28], protect neuronal PC12 cells from high-glucose-induced oxidation and apoptosis [29], and protect neurons against hypoxic neuronal injury [30]
Summary
Glutamate is the major excitatory neurotransmitter in the central nervous system (CNS) [1]. Excessive glutamate can over activate glutamate receptors and result in high calcium ion (Ca2+) influx, which activates a number of enzymes that damage cell structures such as the cell membrane, cytoskeleton components and DNA. This Ca2+ influx is thought to contribute to Ca2+mediated excitotoxic neuronal cell death in the processes of the abovementioned diseases [5]. NMDA receptors are permeable to Na+, K+, and Ca2+ ions, among which excess Ca2+ ions is linearly correlated with NMDA-mediated neuronal cell death triggered by intracellular Ca2+-dependent cascades [7]
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