脱氢表雄酮硫酸酯对体外大鼠脑皮层神经细胞拟老化反应的影响

EFFECTS OF DEHYDROEPIANDROSTERONE SULFATE ONMIMETIC AGING ACTIONS OF CEREBRALCORTEX OF FETAL RATS IN VITRO

用原代培养Ｗｉｓｔａｒ大鼠胎鼠脑皮层神经细胞，从形态学和生化学方面研究自由基、无血清培养对神经元的损伤以及脱氢表雄酮硫酸酯（ＤＨＥＡＳ）的保护作用。结果显示，神经细胞与自由基作用及在无血清培养条件下，细胞生存率明显下降，培养液的上清液中乳酸脱氢酶（ＬＤＨ）活性显著提高，丙二醛（ＭＤＡ）含量明显增加，超氧物岐化酶（ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨＰｘ）活力显著下降。相差显微镜下观察，神经细胞突起回缩，颗粒增加，折光性下降。ＤＨＥＡＳ剂量依赖地提高神经细胞损伤后细胞生存率，降低ＬＤＨ的释放及ＭＤＡ的生成，并显著提高抗氧化酶活性。结果提示，ＤＨＥＡＳ可能通过抑制脂质过氧化物生成及提高抗氧化酶活性来保护拟衰老反应中的大脑皮层神经细胞。

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 μg·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.