| Summary: | 碩士 === 國立成功大學 === 醫學工程研究所碩博士班 === 94 === In the medical clinical, millions die annually from hypoxic- ischemic brain damage due to cerebrovascular disease, subarachnoid hemorrhage, head trauma, shock, and postischemic injury following resuscitation. Neurologic morbidity and mortality are the common consequences because of the lack of efficient therapeutic alternatives. Neuronal death in hypoxia/ischemia injury is a complex event involving failure of metabolic processes, excitotoxicity, loss of calcium homeostasis and oxidative stress, among other factors. They eventually lead to necrotic and/or apoptotic cell death.
Magnolol, an active component extracted from Mognolia officinalis. Meanwhile, M officinalis, as known in Chinese folk medicine as houpo, has long been utilized for treating stomach disorders, cardiovascular and allergic diseases such as thrombosis, bronchial asthma. On the basis of those reported investigations and traditional effect of the herb, it was strongly conceivable that magnolol can be a suitable compound for the development of free radical scavengers (antioxidant).
Among the in vitro systems used to study ischemia-induced injuries, organotypic hippocampal slice cultures, combined with oxygen-glucose deprivation (OGD), offer great advantages in that they mimic closely the situation in vivo. In hippocampal slice cultures, a brief ischemic insult by depriving the cultures of oxygen and glucose can cause a delayed cell death specific to the neuron. Thus, organotypic hippocampal slice cultures combined with OGD could provide a surrogate system for investigation of neuronal cell loss following ischemic injury to the brain.
The results of our study obviously shows that 100μM Magnolol can protect hippocampal neuron cell from dying that suffer from OGD damage. Furthermore, after OGD 4 hours, Magnolol has the ability of repairing neuron cell injury. Unfortunately, OGD 6 hours later, Magnolol could not protect or recover neuron cell damage. Therefore, Magnolol can protect and repair hippocampal neuron cell damage caused by OGD in appropriate concentration and timing.
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