title: Ischemia preconditioning protects rat submandibular glands from ischemia/reperfusion injuries.
abstract: To investigate the effects of ischemia/reperfusion on rat submandibular glands without denervation and the possible protective effects of ischemia preconditioning on the glands that experienced ischemia/reperfusion, in-situ ischemia/reperfusion and ischemia preconditioning experimental models of submandibular glands of healthy male Wistar rats were conducted. For ischemia/reperfusion groups, the glands were subjected to 90 min of ischemia without denervation, followed by 1, 12, 24, or 72 h of reperfusion. Ischemia preconditioning was achieved by 3 min of ischemia following 3 min of reperfusion, performed three times before ischemia/reperfusion. Salivary secretion, histological changes, alterations of tight junctions, myeloperoxidase activity, cellular apoptosis, and reactive oxygen species levels were detected. In ischemia/reperfusion glands, rising acute-inflammation responses, reduced tight-junction width, and increased myeloperoxidase activity, reactive oxygen species levels, and apoptotic cell numbers were observed, along with secretory dysfunction, especially at 1 and 12 h post-reperfusion, which seemed to gradually return to normal by 72 h post-reperfusion. In contrast, ischemia preconditioning showed the potential to ameliorate the injury-stress responses caused by ischemia/reperfusion. Our study revealed that ischemia/reperfusion could cause a series of injury-stress responses and ultimately lead to hyposecretion, independently of the parasympathetic nerve supply, which might play an important role in the early-phase dysfunction of the transplanted glands. Ischemia preconditioning could protect the involved glands and improve ischemia/reperfusion-induced hyposecretion.
authors.affiliation: Department of Oral & Maxillofacial Surgery, Qilu Hospital, and Institute of Dental Medicine, Shandong University, Jinan, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Shi
authors.forename: Meng
authors.initials: M
authors.lastname: Xiao
authors.forename: Mei-Lu
authors.initials: ML
authors.lastname: Dai
authors.forename: Shao-Hua
authors.initials: SH
authors.lastname: Liu
authors.forename: Yun-Sheng
authors.initials: YS
authors.lastname: Liu
authors.forename: Feng-Cai
authors.initials: FC
authors.lastname: Wei
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D004195:Disease Models, Animal; D020287:In Situ Nick-End Labeling; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D046529:Microscopy, Electron, Transmission; D009000:Monocytes / Q000473:pathology; D009504:Neutrophils / Q000473:pathology; D009195:Peroxidase / Q000032:analysis; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000032:analysis; D015427:Reperfusion Injury / Q000517:prevention & control*; D012463:Saliva / Q000378:metabolism; D018987:Salivary Ducts / Q000473:pathology; D012636:Secretory Rate / Q000502:physiology; D013363:Submandibular Gland / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D019108:Tight Junctions / Q000473:pathology; D013997:Time Factors
chemical_list: D017382:Reactive Oxygen Species; D009195:Peroxidase
keywords: ischemic preconditioning; reperfusion injury; secretion