Electroacupuncture preconditioning reduces cerebral ischemic injury via BDNF and SDF-1α in mice.
BACKGROUND
This study was designed to determine if electroacupuncture (EA) preconditioning improves tissue outcome and functional outcome following experimentally induced cerebral ischemia in mice. In addition, we investigated whether the expression of brain-derived neurotrophic factor (BDNF) and stromal cell derived factor-1α (SDF-1α) and infarct volume were related with improvement in neurological and motor function by interventions in this study.


METHODS
After treatment with EA at the acupoints 'Baihui (GV20)' and 'Dazhui (GV14)' for 20 min, BDNF was assessed in the cortical tissues based on Western blot and the SDF-1α and vascular endothelial growth factor (VEGF) levels in the plasma determined by ELISA. To assess the protective effects of EA against ischemic injury, the mice received once a day 20 min EA preconditioning for three days prior to the ischemic event. Focal cerebral ischemia was then induced by photothrombotic cortical ischemia. Infarct volumes, neurobehavioral deficit and motor deficit were evaluated 24 h after focal cerebral ischemia.


RESULTS
The expression of BDNF protein increased significantly from 6 h, reaching a plateau at 12 h after the end of EA treatment in the cerebral cortex. Furthermore, SDF-1α, not VEGF, increased singnificantly from 12 h to 48 h after EA stimulation in the plasma. Moreover, EA preconditioning reduced the infarct volume by 43.5% when compared to control mice at 24 h after photothrombotic cortical ischemia. Consistent with a smaller infarct size, EA preconditioning showed prominent improvement of neurological function and motor function such as vestibule-motor function, sensori-motor function and asymmetric forelimb use. The expression of BDNF colocalized within neurons and SDF-1α colocalized within the cerebral vascular endothelium was observed throughout the ischemic cortex by EA.


CONCLUSIONS
Pretreatment with EA increased the production of BDNF and SDF-1α, which elicited protective effects against focal cerebral ischemia. These results suggest a novel mechanism of EA pretreatment-induced tolerance against cerebral ischemic injury.
Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.
Ji Hyun
JH
Kim
Kyung Ha
KH
Choi
Young Jung
YJ
Jang
Ha Neui
HN
Kim
Sun Sik
SS
Bae
Byung Tae
BT
Choi
Hwa Kyoung
HK
Shin
D015669:Acupuncture Points; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D002545:Brain Ischemia / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D002544:Cerebral Infarction / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D054377:Chemokine CXCL12 / Q000378:metabolism*; D015671:Electroacupuncture; D004730:Endothelium, Vascular / Q000378:metabolism*; D005552:Forelimb; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D019208:Brain-Derived Neurotrophic Factor; D054377:Chemokine CXCL12; D042461:Vascular Endothelial Growth Factor A