Amyloid beta-protein induces apoptosis of neurons in rat hippocampus and expression changes of cyclophilin A in these neurons
10.3760/cma.j.issn.1671-8925.2012.04.003
- VernacularTitle:β-淀粉样蛋白诱导大鼠海马神经元凋亡及海马亲环素A表达的变化
- Author:
Yu-Song GE
1
;
Lin YIN
;
Wei-Yu TENG
;
Chao-Dong ZHANG
Author Information
1. 大连医科大学附属第二医院
- Keywords:
AD;
Amyloid beta-protein;
Cyclophilin A;
Apoptosis
- From:
Chinese Journal of Neuromedicine
2012;11(4):337-341
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the neuron injury in rat hippocampus induced by Aβ25-35 and the cyclophilin A (CyPA) expression changes in these neurons. Methods Sixty healthy Wister rats were equally randomized into experimental group and control group (n=30); AD rat models in the experimental group were established by injection of Aβ25-35 into the bilateral hippocampus of rats,and rats of the control group were received NS injection. The morphological features of neurons in the CA1 area of hippocampus were observed by HE staining; the neuron apoptosis was determined with TUNEL staining; the mRNA and protein expressions of CyPA were detected by PT-PCR and Western blotting,respectively. Results Aβ25-35 caused damage and apoptosis of neurons in the CA1 area of hippocampus; with time being prolonged,the cell injury aggravated and apoptosis increased in the CA1 area ofhippocampus; significant differences were noted as compared with those in control group 1,7 and 14 d after the inducement (P＜0.05).After injection of Aβ25-35 into the hippocampus of rat,the mRNA and protein expressions of CyPA were obviously changed:in early stage,the expressions increased,and then,the expressions decreased gradually; significant differences were noted as compared with those in control group 1 and 7 d after the inducement (P＜0.05); the protein expression of CyPA in the experimental group 14 d after the inducement was significantly decreased as compared with that in the control group (P＜0.05). Conclusion Aβ25-35 plays a neurotoxicity role through aggravating the apoptosis of neurons; and the increment of CyPA expressions maybe play an endogenously protective role in these damage.
