title: [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).
  
  
  CONCLUSIONS
  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.
authors: Zhejiang University of Chinese Medicine, Hangzhou 310005, China.
authors: Jian-Qiao
authors: JQ
authors: Fang
authors: Shu-Xiu
authors: SX
authors: Zhu
authors: Ying
authors: Y
authors: Zhang
authors: Fang
authors: F
authors: Wang
authors: Qing-Yan
authors: QY
authors: Zhu
mesh_terms: D015669:Acupuncture Points; D000544:Alzheimer Disease / Q000201:enzymology / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D000818:Animals; D004195:Disease Models, Animal; D015671:Electroacupuncture; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism*; D006624:Hippocampus / Q000201:enzymology / Q000378:metabolism*; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics* / Q000378:metabolism; D008297:Male; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics* / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D048051:p38 Mitogen-Activated Protein Kinases