Manelli A M, Cadman E D, Shiosaki K, Puttfarcken P S
Neuroscience Discovery, Dept. 47U, Abbott Laboratories, Abbott Park, IL 60064-3500, USA.
Brain Res Bull. 1997;42(3):187-93. doi: 10.1016/s0361-9230(96)00203-1.
To investigate the consequences of complement activation on neuronal viability, the effects of serum treatment on neuron-rich and mixed neuronal/glial cultures were evaluated. The neurotoxicity observed following treatment with either human or rat serum was variable and did not appear to be mediated through a complement-mediated mechanism. Serum lots lacking CH50 activity induced neurotoxicity, and heat treatment of toxic lots of either human or rat sera did not abolish toxicity. In cases where serum treatment did not induce cell death, treatment with PIPLC to remove endogenous membrane-bound complement inhibitors prior to serum exposure, did not result in cell death.
为研究补体激活对神经元活力的影响,评估了血清处理对富含神经元的培养物以及神经元/神经胶质混合培养物的作用。用人血清或大鼠血清处理后观察到的神经毒性各不相同,且似乎不是通过补体介导机制介导的。缺乏CH50活性的血清批次可诱导神经毒性,对人血清或大鼠血清的毒性批次进行热处理并不能消除毒性。在血清处理未诱导细胞死亡的情况下,在血清暴露前用磷脂酰肌醇特异性磷脂酶C(PIPLC)去除内源性膜结合补体抑制剂,并未导致细胞死亡。