Dehydroepiandrosterone (DHEA)

Dehydroepiandrosterone (DHEA) and its sulfate ester, DHEAS, together represent the most abundant steroid hormones in the human body ^[1].

Dehydroepiandrosterone (DHEA) (10-8 and 10-6 M) or DHEAS pretreated rat cerebral cortical cultures was increased neuronal survival when the cultures subjected to anoxia for 2 h ^[2]. When rat cerebral cortical cultures were subjected to anoxia for 2 h in an anaerobic chamber and pretreated with dehydroepiandrosterone (DHEA) (10-8 and 10-6 M) or DHEAS (10-6 M), there was increased neuronal survival. Using cultured neural precursors from rat embryonic forebrains, dehydroepiandrosterone (DHEA) (50 and 100 nM) activated the serine-threonine protein kinase Akt, which is widely implicated in cell survival signaling ^[3].

Dehydroepiandrosterone (DHEA) treating had better locomotor recovery on CD-1 female mice, after contusive spinal cord injury (SCI), and also left-right coordination, and fine motor control than control animals ^[4]. Mice treated with dehydroepiandrosterone (DHEA) also had significantly more white matter spared at the epicenter of the injury and reduced area of reactive gliosis surrounding the lesion. Dehydroepiandrosterone (DHEA) treatment was intensive and consisted of three different modes of administration: a DHEA Matrigel patch (10-10 M) applied to the spinal cord before closure of the wound, followed by 12 days of i.p. injections of saline containing Dehydroepiandrosterone (DHEA) (10-6 M or 0.02 mg/kg/day) after SCI, and Dehydroepiandrosterone (DHEA) (10-6 M) in the drinking water for 42 days ^[4].

References:
[1]. Rice SP, Zhang L, Grennan-Jones F, Agarwal N, Lewis MD, Rees DA, Ludgate M: Dehydroepiandrosterone (DHEA) treatment in vitro inhibits adipogenesis in human omental but not subcutaneous adipose tissue. Mol Cell Endocrinol 2010, 320: 51-57. 10.1016/j.mce.2010.02.017
[2]. C.E. Marx, L.F. Jarskog, J.M. Lauder, J.H. Gilmore, J.A. Lieberman, A.L. Morrow. Neurosteroid modulation of embryonic neuronal survival in vitro following anoxia. Brain Res., 871 (2000), pp. 104-112
[3]. L. Zhang, B. Li, W. Ma, J.L. Barker, Y.H. Chang, W. Zhao, D.R. Rubinow. Dehydroepiandrosterone (DHEA) and its sulfated derivative (DHEAS) regulate apoptosis during neurogenesis by triggering the Akt signaling pathway in opposing ways. Brain Res. Mol. Brain Res., 98 (2002), pp. 58-66
[4]. C. Fiore, D.M. Inman, S. Hirose, L.J. Noble, T. Igarashi, N.A. Compagnone. Treatment with the neurosteroid dehydroepiandrosterone promotes recovery of motor behavior after moderate contusive spinal cord injury in the mouse. J. Neurosci. Res., 75 (2004), pp. 391-400

脱氢表雄酮 (DHEA) 及其硫酸酯 DHEAS 共同代表了人体内最丰富的类固醇激素^[1]。

脱氢表雄酮 (DHEA)（10- 8 和 10-6 M) 或 DHEAS 预处理的大鼠大脑皮层培养物在缺氧 2 小时后神经元存活率增加 ^[2]。当大鼠大脑皮质培养物在厌氧室中缺氧 2 小时并用脱氢表雄酮 (DHEA)（10-8 和 10-6 M）或 DHEAS（10-6 M）预处理时,神经元存活率增加。使用来自大鼠胚胎前脑的培养神经前体,脱氢表雄酮 (DHEA)（50 和 100 nM）激活丝氨酸-苏氨酸蛋白激酶 Akt,后者广泛参与细胞存活信号转导^[3]。

在挫伤性脊髓损伤 (SCI) 后,脱氢表雄酮 (DHEA) 治疗对 CD-1 雌性小鼠的运动恢复、左右协调和精细运动控制均优于对照动物^{[4]。用脱氢表雄酮 (DHEA) 治疗的小鼠在损伤中心也有明显更多的白质,并且损伤周围的反应性神经胶质增生区域减少。脱氢表雄酮 (DHEA) 治疗是强化治疗,由三种不同的给药方式组成:在伤口闭合前将 DHEA Matrigel 贴剂 (10-10 M) 应用于脊髓,然后进行 12 天的腹膜内注射。脊髓损伤后注射含脱氢表雄酮（DHEA）（10-6 M 或 0.02 mg/kg/天）的生理盐水,并在饮用水中注射脱氢表雄酮（DHEA）（10-6 M）42天[4].}