title: Electroacupuncture ST36 prevents postoperative intra-abdominal adhesions formation.
abstract: BACKGROUND
  We have recently proved electroacupuncture (EA) ST36 exerted an anti-inflammatory effect in the early phase of intra-abdominal adhesion formation. Evidences indicate that the anti-inflammatory effect of EA ST36 involves a cholinergic anti-inflammatory pathway-dependent mechanism via the vagus nerve. However, the exact effects and accurate vagal modulation of acupuncture in prevention of postoperative intra-abdominal adhesion formation has not been thoroughly evaluated.
  
  
  METHODS
  Sprague-Dawley rats subjected to abdominal adhesion lesions operation at the cecum and abdominal wall were randomly divided into six groups as follows: (a) EAN: EA non-channel acupoints; (b) EA: EA ST36 after abdominal lesions; (c) VGX/EA: vagotomy (VGX) after abdominal lesions, then EA ST36; (d) VGX/EAN: VGX after abdominal lesions, then EAN; (e) α-BGT/EA: intraperitoneal injection of α-bungarotoxin (α-BGT, an antagonist of α7 subunit of cholinergic nicotinic receptor) before EA ST36, and (f) α-BGT/EAN group: α-BGT injection before EAN. Seven days after abdominal surgical lesions, the levels of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in the adhesive tissue were evaluated, macroscopic observation and histopathologic evaluation of adhesion formation and assessment of angiogenesis by immunohistochemical staining of platelet endothelial cell adhesion molecule-1 (CD31) were performed.
  
  
  RESULTS
  EA ST36 reduced TNF-α and VEGF levels in adhesive tissue homogenates 7 d after surgery, whereas vagotomy or intraperitoneal injection of α-BGT before EA ST36 reversed its suppressive effects. EA at non-channel acupoints with or without vagotomy or intraperitoneal injection of α-BGT before EA had no suppressive effects on TNF-α and VEGF levels. EA ST36 alleviated the adhesion formation, with both of macroscopic and histopathologic adhesion scores significantly lower than those of the EAN group (1.56 ± 0.29 versus 3.00 ± 0.82, 1.35 ± 0.4 versus 3.91 ± 0.8, respectively, both P < 0.05). Compared with the EAN group, EA ST36 significantly decreased angiogenesis evidenced by reduced CD31 positive microvessel density in adhesive tissue.
  
  
  CONCLUSIONS
  EA ST36 might reduce the postoperative local inflammatory response, attenuate the angiogenesis, and alleviate the adhesion formation partly via activating the cholinergic anti-inflammatory mechanism.
authors.affiliation: Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China; Department of Pediatric Orthopedic Surgery, Chinese PLA General Hospital, Beijing, China.
authors.forename: Ming-Hua
authors.initials: MH
authors.lastname: Du
authors.affiliation: Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China; Department of Burns, Guangdong General Hospital, Guangzhou, China.
authors.forename: Hong-Min
authors.initials: HM
authors.lastname: Luo
authors.affiliation: Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China.
authors.forename: Yi-Jun
authors.initials: YJ
authors.lastname: Tian
authors.affiliation: Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China.
authors.forename: Li-Jian
authors.initials: LJ
authors.lastname: Zhang
authors.affiliation: Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China.
authors.forename: Zeng-Kai
authors.initials: ZK
authors.lastname: Zhao
authors.affiliation: Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Lv
authors.affiliation: Department of Pediatric Orthopedic Surgery, Chinese PLA General Hospital, Beijing, China.
authors.forename: Rui-Jiang
authors.initials: RJ
authors.lastname: Xu
authors.affiliation: Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China. Electronic address: bs0425@163.com.
authors.forename: Sen
authors.initials: S
authors.lastname: Hu
mesh_terms: D058107:Abdominal Wound Closure Techniques; D000818:Animals; D002432:Cecum / Q000473:pathology; D015671:Electroacupuncture; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control; D008297:Male; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000517:prevention & control; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D000267:Tissue Adhesions / Q000473:pathology / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat
keywords: Abdominal adhesions; Angiogenesis; Electroacupuncture; Inflammation; ST36