[Effect of electroacupuncture on expression of phosphorylated P 38 MAPK and IL-1beta in frontal lobe and hippocampus in rats with Alzheimer's disease]

Abstract

Objective: To observe the effect of electroacupuncture (EA) intervention on expression of phosphorylated mitogen activated protein kinase-P 38 (p-P 38 MAPK) protein and Interleukin 1beta (IL-1beta)mRNA in the frontal lobe and hippocampus in Alzheimer's disease (AD) rats so as to explore its mechanisms underlying improvement of AD in clinic.

Methods: Thirty-two SD rats were equally and randomly divided into normal control (normal), sham-operation (sham), model and EA groups. AD model was established by microinjection of Abeta(1-40) (10 microg/microL, 1 microL) into bilateral Meynert nucleus (AP: 1. 4 mm, L: 3 mm, H: 7 mm) and validated by water maze tests. Rats of the sham group were treated by microinjection of the same dose of normal saline into the bilateral Meynert Nucleus. EA (1 mA, 2 Hz) was applied to bilateral "Baihui" (GV 20), "Taixi" (KI 3) and "Zusanli" (ST 36) for 15 min, once daily for 12 sessions. Expression levels of p-P 38 MAPK protein and IL-1beta mRNA in the hippocampus and frontal lobe tissues were detected by Western blot and RT-PCR, respectively.

Results: In comparison with the normal group, the expression levels of p-P 38 MAPK protein and IL-1beta mRNA in the hippocampus and frontal lobe tissues were upregulated significantly in the model group (P < 0.01). After 12 sessions of EA intervention, the expression levels of both p-P 38 MAPK protein and IL-1beta mRNA were down-regulated significantly (P < 0.01, P < 0.05) in spite of being still higher than those of the normal group. No significant differences were found between the normal and sham groups in the expression levels of both p-P 38 MAPK protein and IL-1beta mRNA (P > 0.05).

Conclusion: EA intervention can reduce the over expression of both p-P 38 MAPK protein and IL-1beta mRNA in the hippocampus and frontal cortex in AD rats, suggesting an improvement of AD after EA intervention by restraining the inflammatory reaction.