4725-51-3Relevant articles and documents
Sulfuric acid hydrolysis of 3-beta-hydroxy-5-alpha, 6-alpha-epoxyandrostane.
Weinman,Weinman
, p. 699 - 705 (1965)
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2?,3a,5a-TRIHYDROXY-ANDROST-6-ONE AND PREPARATION METHODS AND USE THEREOF
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, (2016/03/05)
The present invention discloses compound 2β,3α,5α-trihydroxy-androst-6-one, having the structure of formula (I). The present invention also discloses a plurality of methods for preparing the compound and a use of the compound.
A synthetic steroid 5α-Androst-3β,5,6-Triol blocks hypoxia/reoxygenation - Induced neuronal injuries via protection of mitochondrial function
Chen, Jiesi,Leng, Tiandong,Chen, Wenli,Yan, Min,Yin, Wei,Huang, Yijun,Lin, Suizhen,Duan, Dayue,Lin, Jun,Wu, Gongxiong,Zhang, Jingxia,Yan, Guangmei
, p. 996 - 1002 (2013/10/21)
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.