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  • Title: A synthetic steroid 5α-androst-3β,5,6β-triol blocks hypoxia/reoxygenation-induced neuronal injuries via protection of mitochondrial function.
    Author: Chen J, Leng T, Chen W, Yan M, Yin W, Huang Y, Lin S, Duan D, Lin J, Wu G, Zhang J, Yan G.
    Journal: Steroids; 2013 Oct; 78(10):996-1002. PubMed ID: 23811019.
    Abstract:
    Ischemic stroke is a leading cause of death worldwide, yet therapies are limited. During periods of ischemia following reperfusion in ischemic stroke, not only loss of energy supply, but a few other factors including mitochondrial dysfunction and oxidative stress also make vital contribution to neuronal injury. Here we synthesized a steroid compound 5α-androst-3β,5,6β-triol by 3 steps starting from dehydroepiandrosterone and examined its effect on mitochondrial function and oxidative stress in primary cultured cortical neurons exposed to hypoxia followed by reoxygenation. 5α-Androst-3β,5,6β-triol dose-dependently protected cortical neurons from hypoxia/reoxygenation exposure. Rates of reduction in neuronal viability, loss of mitochondrial membrane potential, disruption of ATP production and oxidative stress were ameliorated in 5α-androst-3β,5,6β-triol pretreated cultures. In summary, these results suggest that 5α-androst-3β,5,6β-triol is neuroprotective against hypoxia/reoxygenation induced neuronal injuries through mediation of mitochondrial function and oxidative stress.
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