title: [Study of effect of tongsaimai tablets on experimental diabetic foot model rats].
abstract: OBJECTIVE
  To observe the effect of Tongsaimai (TSM) tablets in treating foot trauma of diabetic foot (DF) model rats, and discuss its potential mechanism.
  
  
  METHODS
  Male SD rats were selected to duplicate the diabetic foot ulcer model and randomly divided into the blank control group, the model group, the metformin treatment group, and TSM 12.44, 6.22, 3.11 g x kg(-1) groups (n = 10). The healing of ulcer wounds were observed on day 1, 4, 8, 13 and 18. After 18 days, a histopathologic examination was conducted for ulcer tissues. The contents of superoxide dismutase (SOD) and malondialdehyde (MDA) were detected by hydroxylamine and TBA methods. The content of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were determined with the radioimmunoassay. The immunohistochemical method was used to observe the expression of vascular endothelial growth factor (VEGF) in ulcer tissues and the number of capillary vessels.
  
  
  RESULTS
  TSM could alleviate the pathological changes of diabetic foot rats, accelerate the ulcer healing on 4, 8, 13, 18 d, reduce MDA, IL-6, TNF-alpha, VEGF content in rat serum at 18 d (after the rehabilitation period), and enhance the SOD content. Specifically, the TSM 12.44 g x kg(-1) group showed significant differences compared with the model group (P < 0.05, P < 0.01). At 18 d after the treatment (the late rehabilitation period), the VEGF expression of TSM 12.44, 6.22 g x kg(-1) groups and the number of blood capillaries of the TSM 12.44 g x kg(-1) group were significantly lower than that of the model group (P < 0.05, P < 0.01).
  
  
  CONCLUSIONS
  TSM could promote the foot wound healing of DF model rats, reduce MDA, IL-6 and TNF-alpha levels in serum, increase the SOD content and decrease the VEGF expression and the number of blood capillaries in the late rehabilitation period. Its action mechanism may be related to the inhibition of oxidative stress injury and the inflammatory cell infiltration.
authors.forename: Jing
authors.initials: J
authors.lastname: Guo
authors.forename: Qing-Hai
authors.initials: QH
authors.lastname: Meng
authors.forename: Qiu-Yi
authors.initials: QY
authors.lastname: Yin
authors.forename: Chao
authors.initials: C
authors.lastname: Lin
authors.forename: Zhi
authors.initials: Z
authors.lastname: Ma
authors.forename: Bin
authors.initials: B
authors.lastname: Xu
authors.forename: Xing
authors.initials: X
authors.lastname: Qian
authors.forename: Dong-Qiao
authors.initials: DQ
authors.lastname: Bao
authors.forename: Ya-Yun
authors.initials: YY
authors.lastname: Zhang
authors.forename: Qi-Chun
authors.initials: QC
authors.lastname: Zhang
authors.forename: Hui-Min
authors.initials: HM
authors.lastname: Bian
authors.forename: Xiao-Ying
authors.initials: XY
authors.lastname: Hu
mesh_terms: D000818:Animals; D017719:Diabetic Foot / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage*; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D013607:Tablets / Q000008:administration & dosage; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects
chemical_list: D004365:Drugs, Chinese Herbal; D015850:Interleukin-6; D013607:Tablets; D042461:Vascular Endothelial Growth Factor A; D008315:Malondialdehyde; D013482:Superoxide Dismutase