title: Ischemic preconditioning reduces transplanted submandibular gland injury.
abstract: BACKGROUND
  Ischemic preconditioning (IPC) can reduce ischemia/reperfusion (I/R) injury in multiple organs and species. However, the effect of IPC on transplanted submandibular glands remains unknown. We explored the protection of IPC in transplanted submandibular glands in the rabbit and the underlying mechanism.
  
  
  METHODS
  IPC was performed by clamping the lingual artery for 10 min, with 10 min of reperfusion before transplantation. Male rabbits were randomly divided into control, transplantation, and IPC groups (n = 6 each). Saliva secretion, oxidative stress, pro-inflammatory cytokine levels, and apoptosis-related protein levels were determined at 1, 12, and 24 h after reperfusion.
  
  
  RESULTS
  Salivary flow was significantly increased at 12 h and decreased at 24 h in the transplanted glands. IPC treatment prevented the reduced saliva secretion at 24 h after reperfusion (P < 0.01). The mRNA levels of tumor necrosis factor-α, interleukin-1β, and reactive oxygen species, as well as malondialodehyde (MDA) and myeloperoxidase activity, were significantly increased and superoxide dismutase activity was decreased in the transplanted glands. However, these changes were all attenuated with IPC treatment (all P < 0.05). Also, acinar cell apoptosis and Bax protein expression were decreased and Bcl-2 protein expression was increased in the IPC-treated glands at 1 and 12 h after reperfusion (all P < 0.05).
  
  
  CONCLUSIONS
  IPC protects the secretory function of transplanted submandibular gland in the rabbit by reducing the inflammatory response, attenuating oxidative stress, and an anti-apoptosis process.
authors.affiliation: Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, Beijing, People's Republic of China.
authors.forename: Ning-Yan
authors.initials: NY
authors.lastname: Yang
authors.forename: Liang
authors.initials: L
authors.lastname: Shi
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Chong
authors.initials: C
authors.lastname: Ding
authors.forename: Xin
authors.initials: X
authors.lastname: Cong
authors.forename: Feng-Ying
authors.initials: FY
authors.lastname: Fu
authors.forename: Li-Ling
authors.initials: LL
authors.lastname: Wu
authors.forename: Guang-Yan
authors.initials: GY
authors.lastname: Yu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D007249:Inflammation / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D019194:Ischemic Preconditioning; D008297:Male; D023421:Models, Animal; D018384:Oxidative Stress / Q000502:physiology*; D009195:Peroxidase / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000378:metabolism; D012463:Saliva / Q000378:metabolism*; D013363:Submandibular Gland / Q000378:metabolism / Q000473:pathology* / Q000637:transplantation*; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D009195:Peroxidase; D013482:Superoxide Dismutase