Wang Y, Rao M
Department of Cardiovascular Pharmacology, Nanjing Medical University, Nanjing 210029.
Yao Xue Xue Bao. 1998 Jun;33(6):413-7.
The effects of dehydroepiandrosterone sulfate (DHEAS) on mimetic aging action of cultured neurons were studied in two models: the cultured cerebral cortex neurons were exposed to the xanthine oxidase-hypoxanthine(XO-HPX) system; serum free culture of cerebral cortex neurons. The results indicated that when cultured neurons were incubated for 6 h with XO-HPX system or 24 h serum free cultures, LDH release and MDA content increased while the number of surviving neurons decreased. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased and morphological injury developed. DHEAS (25, 50, 100 micrograms.L-1) concentration-dependently increased the number of surviving neurons and the activities of SOD and GSH-Px. It also inhibited the elevation of LDH and MDA induced by free radical and serum free cultures. The results suggest that DHEAS prevent the toxicity of free radical and serum free culture insults by suppressing the generation of lipid peroxide and increasing the activities of antioxidant enzymes.
在两种模型中研究了硫酸脱氢表雄酮（DHEAS）对培养神经元模拟衰老作用的影响：将培养的大脑皮质神经元暴露于黄嘌呤氧化酶-次黄嘌呤（XO-HPX）系统；大脑皮质神经元的无血清培养。结果表明，当培养的神经元与XO-HPX系统孵育6小时或进行24小时无血清培养时，乳酸脱氢酶（LDH）释放和丙二醛（MDA）含量增加，而存活神经元数量减少。超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性降低，并且出现形态学损伤。DHEAS（25、50、100微克·升-1）呈浓度依赖性增加存活神经元的数量以及SOD和GSH-Px的活性。它还抑制自由基和无血清培养诱导的LDH和MDA升高。结果表明，DHEAS通过抑制脂质过氧化物的产生并增加抗氧化酶的活性来预防自由基毒性和无血清培养损伤。
