β-淀粉样蛋白对培养神经细胞的毒性作用及神经节苷脂的保护作用

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向培养液中加入15mmol/L的β-AP1-40,48h后,发现原代培养的海马细胞内Ca2+的浓度明显增高,对照组为23.9±3.6(n=51)而β-AP组为36.5±15.8(n=30),两组比较P<0.001,有非常显著性的差别。对照组的乳酸脱氢酶没有明显变化,而β-AP组在加β-AP1-4048h后乳酸脱氢酶明显增加,从52iu/L增加到105iu/L,实增加了101%。实验结果表明,β-AP1-40对培养的神经细胞有明显的毒性作用,但没有发现形态学的变化和对细胞的特异性。如在培养液中加β-AP1-40的同时再加25mg/ml的神经节苷脂(GAs)可明显减弱β-AP1-40引发的胞内Ca2+浓度和培养液中LDH浓度的升高。β-AP+GAs组胞内Ca2+浓度为27.7±5.58,与β-AP组比较,有显著性差异(P<0.01)。β-AP组海马细胞培养液中乳酸脱氢酶的浓度增高为101%,而β-AP-GAs组培养液中乳酸脱氢酶的浓度增高仅为67%。在NG108-15细胞上也获得了相同的结果。单唾液酸神经节苷脂虽有与GAs类似的作用,但较弱。这些实验结果指出,神经节苷脂和单唾液酸神经节苷脂均能拮抗β-AP1-40的毒性作用,从而对细胞可起到保护作用。 The concentration of Ca2 + in primary cultured hippocampal cells was significantly increased after adding 15mmol / L β-AP1-40 for 48h to the culture medium, the control group was 23.9 ± 3.6 (n = 51) AP group was 36.5 ± 15.8 (n = 30), the two groups were P <0.001, there is a very significant difference. Lactate dehydrogenase in the control group did not change significantly, while in the β-AP group, lactate dehydrogenase increased significantly from 52iu / L to 105iu / L after adding β-AP for 1-4048h, an increase of 101%. The experimental results showed that β-AP1-40 had obvious toxic effects on cultured nerve cells, but no morphological changes and cell specificity were found. Adding β-AP1-40 and 25mg / ml gangliosides (GAs) to culture medium could significantly reduce the intracellular Ca2 + concentration induced by β-AP1-40 and the increase of LDH concentration in culture medium. The intracellular Ca2 + concentration in β-AP + GAs group was 27.7 ± 5.58, which was significantly different from that in β-AP + GAs group (P <0.01). The concentration of lactate dehydrogenase in hippocampal cell culture fluid of β-AP group was increased by 101%, while the concentration of lactate dehydrogenase in β-AP-GAs group culture medium was only increased by 67%. The same result was also obtained on NG108-15 cells. Monosialogangliosides, although similar to GAs, are weaker. These experimental results indicate that both gangliosides and monosialogangliosides can antagonize the toxic effects of β-AP1-40 and thus have a protective effect on the cells.
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