[β-淀粉样蛋白通过增加活性氧生成上调晚期糖基化终产物受体的表达]
[β-amyloid protein up-regulates the expression of the receptor for advanced glycation end products by increasing ROS production].
作者信息
Kong Weina, Zhang Jia, Gao Weijuan, Liu Qingtao, Zhou Liming, Chai Xiqing
机构信息
Bioreactor and Protein Drug Research and Development Center of Hebei Universities, Hebei Chemical and Pharmaceutical College, Shijiazhuang 050026, China. E-mail:
出版信息
Nan Fang Yi Ke Da Xue Xue Bao. 2013 Aug;33(8):1132-6.
OBJECTIVE
To investigate the mechanism of β-amyloid protein (Aβ) in regulating the expression of the receptor for advanced glycation end products (RAGE).
METHODS
Aβ1-40 was injected into the bilateral hippocampus of rats, and 3 weeks later, the levels of reactive oxygen species (ROS) production were detected by flow cytometry. The expressions of RAGE, reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (gp9l(phox) and p47(phox)), nuclear factor-κB (NF-κB), and inhibitor of κB (IκB) were measured by Western blotting.
RESULTS
Injection of Aβ1-40 caused a significant increase in the expressions of RAGE, gp9l(phox), p47(phox), phospho-p47(phox), phospho-IκBα, NF-κB and phospho-NF-κB in rat hippocampus but decreased the level of IκBα. Aβ1-40 injection also resulted in a significantly increased content of ROS in the hippocampus of the rats.
CONCLUSION
Aβ up-regulates the expression of RAGE in rat hippocampus via NADPH/ ROS/NF-κB signaling pathway.
目的
探讨β-淀粉样蛋白（Aβ）调节晚期糖基化终末产物受体（RAGE）表达的机制。
方法
将Aβ1-40注入大鼠双侧海马，3周后，通过流式细胞术检测活性氧（ROS）生成水平。采用蛋白质免疫印迹法检测RAGE、还原型烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶（gp9l(phox)和p47(phox)）、核因子-κB（NF-κB）及κB抑制蛋白（IκB）的表达。
结果
注射Aβ1-40导致大鼠海马中RAGE、gp9l(phox)、p47(phox)、磷酸化p47(phox)、磷酸化IκBα、NF-κB及磷酸化NF-κB的表达显著增加，但IκBα水平降低。注射Aβ1-40还导致大鼠海马中ROS含量显著增加。
结论
Aβ通过NADPH/ROS/NF-κB信号通路上调大鼠海马中RAGE的表达。
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