Wang Ju-Yu, Shum Andrew Y-C, Wang Jia-Yi
Department of Basic Medical Science, Hung-Kuang Institute of Technology, Sha-Lu, Taichung, Taiwan.
Neurosci Lett. 2002 Apr 12;322(3):187-91. doi: 10.1016/s0304-3940(02)00102-7.
Hypoxia/reoxygenation (H/R) causes cell injury/death. We examined the protection by drugs intervening at various stages of the injury cascade in cultured neurons and glia. Primary cultures of rat cortical neurons and mixed glia were subjected to H/R. Measurements of cell death (by lactate dehydrogenase release into the medium) and viability (by MTT reduction) indicated that H/R led to time-dependent injury in both neuronal and mixed glial cultures. The extent of cell injury in neurons was significantly greater than in glia cells. Pretreatment with (+)-MK-801 hydrogen maleate (MK-801) (an N-methyl-D-aspartate antagonist), N(omega)-nitro-L-arginine methyl ester (L-NAME) (an inhibitor of nitric oxide synthase) or free radical scavengers reduced the extent of the H/R-elicited neuronal damage. MK-801, in contrast, was without effect on glial cells while L-NAME was effective. Our results suggest differential mechanism(s) and susceptibility to injury caused by H/R for neurons and mixed glia.
缺氧/复氧（H/R）会导致细胞损伤/死亡。我们研究了在培养的神经元和神经胶质细胞中，药物干预损伤级联反应各个阶段所提供的保护作用。对大鼠皮质神经元和混合神经胶质细胞进行原代培养，并使其经历H/R。通过测量细胞死亡（通过乳酸脱氢酶释放到培养基中的量）和细胞活力（通过MTT还原）表明，H/R在神经元和混合神经胶质细胞培养物中均导致时间依赖性损伤。神经元中的细胞损伤程度明显大于神经胶质细胞。用马来酸氢（+）-MK-801（MK-801，一种N-甲基-D-天冬氨酸拮抗剂）、N（ω）-硝基-L-精氨酸甲酯（L-NAME，一种一氧化氮合酶抑制剂）或自由基清除剂进行预处理可降低H/R引发的神经元损伤程度。相比之下，MK-801对神经胶质细胞没有影响，而L-NAME则有效。我们的结果表明，神经元和混合神经胶质细胞对H/R所致损伤的机制和易感性存在差异。
