title: A New Approach of Short Wave Protection against Middle Cerebral Artery Occlusion/Reperfusion Injury via Attenuation of Golgi Apparatus Stress by Inhibition of Downregulation of Secretory Pathway Ca(2+)-ATPase Isoform 1 in Rats.
abstract: BACKGROUND
  Short wave (SW), a pattern of electromagnetic therapy, achieves an oscillating electromagnetic field. It has been reported that it may have a potential effect on cerebral injury. The present study was designed to investigate the potential role and possible mechanism of SW in focal cerebral ischemia/reperfusion (I/R) injury in rats. Secretory pathway Ca(2+)/Mn(2+) ATPase isoform 1 is a major component of Golgi apparatus stress. It has been reported as representative of Golgi apparatus stress.
  
  
  METHODS
  Up to 120 minutes of middle cerebral artery occlusion (MCAO) and reperfusion injury was induced in male Sprague-Dawley rats. Different sessions of SW daily were administered over head after reperfusion from day 1 to day 7. Functional recovery scores, survival rates, infarct volume analysis, electron microscope test, and western blotting studies were used to analyze the therapy.
  
  
  RESULTS
  SW protected against neuronal death and apoptosis in cornu ammon 1 region of hippocampus by reducing neuronal deficit, infarct volume, and ultrastructure. SW partly inhibited upregulation of caspase3. In addition, the expression of secretory pathway Ca(2+)-ATPase isoform 1 (SPCA1) was upregulated by SW.
  
  
  CONCLUSIONS
  Our data indicate that SW can be protected against focal cerebral I/R injury, and the influence on Golgi apparatus stress might provide us a new perspective in further study. To the authors' knowledge, this is the first report using SW to increase expression of SPCA1 indicating modulate Golgi apparatus stress in MCAO and reperfusion model.
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Yongmei
authors.initials: Y
authors.lastname: Fan
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Changjie
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Li
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Wenna
authors.initials: W
authors.lastname: Peng
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Yin
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Xiaofao
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Kong
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Chunna
authors.initials: C
authors.lastname: Lan
authors.affiliation: Department of Rehabilitation, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
authors.forename: Rumi
authors.initials: R
authors.lastname: Wang
authors.affiliation: Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China. Electronic address: huzhiping2014@163.com.
authors.forename: Zhiping
authors.initials: Z
authors.lastname: Hu
mesh_terms: D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000201:enzymology* / Q000503:physiopathology / Q000648:ultrastructure; D020013:Calcium Signaling; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D006056:Golgi Apparatus / Q000201:enzymology* / Q000648:ultrastructure; D020244:Infarction, Middle Cerebral Artery / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D009474:Neurons / Q000201:enzymology* / Q000648:ultrastructure; D018696:Neuroprotective Agents / Q000494:pharmacology*; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D012780:Short-Wave Therapy; D013997:Time Factors; D015854:Up-Regulation
chemical_list: C492023:Atp2c1 protein, rat; D004791:Enzyme Inhibitors; D018696:Neuroprotective Agents; C505410:Casp3 protein, rat; D053148:Caspase 3; D000252:Calcium-Transporting ATPases
keywords: Cerebral ischemia/reperfusion injury; Golgi apparatus stress; MCAO reperfusion; SPCA1; electromagnetic fields; short wave