摘要
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。
Primary cultured hippocampal cells and NG108-15 cells were used in experiments. Forty eight hours after adding 15 μmol/L β-AP1-40 to culture medium, the intracellular Ca2+ concentration increased significantly. The Ca2+ concentrations of cultured hippocampal cells in control group and β-AP group were 23. 9±3. 6 (n= 51 ) and 36. 5±15. 8 (n=30) respectively (P<0.001). The level of LDH concentration in culture medium was obviously raised at 101% by administration of β-AP. Although no morphological change was found. The similar result was obtained from NG108-15 cells. Moreover, high concentration of intracellular Ca2+ and LDH culture medium were decreased by gangliosides (GAs) or GM1 (25 mg/ml). The Ca2+ concentration of βAP treated group of hippocampal cells was 36. 5 ± 15. 8, but that of β-AP+GAs group was 27. 7 ± 5. 58 (P<0. 01 ). The increased LDH concentration in culture medium of β-AP group was decreased by GAs from 101 % to 67 %. GM1 has the same effcet that seems a little weaker than the effect of GAs. These results show that gangliosides have certain protecting effect on cultured nerve cells from toxicity of β-AP.
出处
《神经解剖学杂志》
CSCD
北大核心
1998年第4期303-308,共6页
Chinese Journal of Neuroanatomy
基金
国家自然科学基金