| 李馨敏 施晴 于丰祥 宫平 冯雪梅 祁红 李娟△.Abeta-Cu 复合物与Abeta纤丝对小胶质细胞激活作用比较研究[J].,2016,16(23):4401-4405 |
| Abeta-Cu 复合物与Abeta纤丝对小胶质细胞激活作用比较研究 |
| Comparison of the Effects on Microglial Activation by A beta-Cu Complex andFibrillar A beta* |
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| DOI： |
| 中文关键词: 阿尔茨海默病 Cu2+ Aβ Aβ-Cu 复合物 |
| 英文关键词: Alzheimer's Disease Cu2+ Aβ Abeta-Cu complex |
| 基金项目:国家自然科学基金项目（30973538，81373417） |
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| 中文摘要: |
| 目的：比较具有氧化还原活性的过渡金属离子Cu2+(Cu)诱导形成的A茁聚集物（Aβ-Cu 复合物）与Aβ自聚集形成的纤丝
（Fibrillar Aβ, fAβ）对小胶质细胞激活作用的差异。方法：制备Aβ-Cu复合物和fAβ，利用小鼠BV-2 小胶质细胞株，分别以不同浓
度的Aβ-Cu 复合物和fAβ于37 ℃刺激24 h，检测细胞上清液中的TNF-α（Tumor necrosis factor-α）、NO（Nitric oxide）以及H2O2
（Hydrogen Peroxide）的含量。分别收集Aβ-Cu复合物和fA茁作用24 h 后的大鼠原代小胶质细胞条件培养液，通过观察该条件培
养液对大鼠原代海马神经元细胞活力的影响，评价小胶质细胞介导的间接神经元毒性。结果：（1）在不引起直接神经毒性剂量
（2.5 uM）下，Aβ-Cu 复合物激活小胶质细胞释放TNF-alpha（P<0.01）、NO（P<0.05）以及H2O2（P<0.05）的作用强于fAβ。（2）在此剂量
下，A茁-Cu 复合物通过激活小胶质细胞引起的间接神经元毒性强于fAβ（P<0.05）。结论：与fAβ相比，非神经毒性剂量的Aβ-Cu
复合物对于小胶质细胞具有更强的激活作用，并由此引发更为明显的神经元毒性。 |
| 英文摘要: |
| Objective:To compare the effects of Abeta-Cu complex with fibrillar Abeta(fAβ) on microglial activation.Methods:fAβ
was prepared by dissolving Aβ1-40 in ddH2O, which was followed by incubation at 37 ℃ for 7 days. Aβwas incubated with Cu2+(Cu) at an
equimolar ratio to obtain the Aβ-Cu complex. BV-2 microglial cells were treated with Aβ-Cu and fAβ. The TNF-αand nitric oxide levels
in the media were determined and cell viability was measured as well. Extracellular hydrogen peroxide was quantified by fluorometric
assay with Amplex Red. The conditioned mediumof Aβ-Cuactivated and fAβ-activated microglia was collected, and the microglia-mediated
neurotoxicity was observed.Results:Without causing neuronal cell toxicity, compared with fAβ, the activation effect of Aβ-Cu
complex on microglial cells was stronger, releasing more TNF-α(P<0.01), nitric oxide (P<0.05) and hydrogen peroxide (P<0.05). In addition,
the conditioned medium of Aβ-Cu complex-treated microglia could cause more obvious neurotoxicity than that of fAβ(P<0.05).Conclusion:Compared with fAβ, Aβ-Cu complex has a stronger effect on microglial activation and microglia-mediated neurotoxicity. |
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