Objective: To investigate the influence of heat shock (HS) preconditioning on the ultra-structure of gastric mucosal cells and the activity of cytochrome oxidase (CCO) and superoxide dismutase (SOD) in mitochondria isolated from gastric mucosa of burned rats in order to investigate its protective mechanism on burn-induced acute gastric mucosal lesion.
Methods: Ninety-six Wistar rats were divided randomly into two groups:(1) burn model group (n =40) undergoing burning and made into model of acute gastric mucosal lesion; and then subdivided into 5 equal subgroups: 3, 6, 12, 24, and 48 h after burning; (2) normal control group (n = 8); (3) HS preconditioning + burn group (n = 40), undergoing burning 24 h after HS preconditioning; and (4) HS preconditioning group (n = 8), without burn as experimental control A number of rats were sacrificed and laparotomized before and 3, 6, 12, 24, and 48 h after the burning. Specimens were obtained from the gastric antrum, bodies if stomach and gastric lesion to undergo microscopy and determination of the ulcer index ( UI ). Streptavidin-peroxidase immunohistochemistry was used to detect the protein expression of heat shock protein (HSP)-60 and HSP-70. Mitochondria were isolated and the activities of CCO and SOD in mitochondria were measured. The dynamic postburn changes in micro and ultra structure of gastric mucosal cells of scalded rats were observed.
Results: The rats of the burn group showed conspicuous gastric mucosal lesions. The UI levels at every time point of the HS group were all the lowest in comparison with other groups. The expression levels of HSP70 and HSP60 of the HS group, especially those at the time points 3, 6, 12, and 24 h were significantly higher than those of the burn group (P <0.05 or P <0.01). The activities of mCCO and mSOD of the HS group did not decrease remarkably at any time point in comparison with the control groups, and the activities of mCCO and mSOD at the time points 6, 12, and 24 h of the HS group were all significantly higher than those of the burn group (P <0.05 of P <0.01). Electron microscopy showed that the ultrastructural lesion was mild and alteration of gastric mucosal mitochondria was not significant in the HS group compared with those of the burn group. A positive correlation was shown between SOD and HSP70 (r = 0.436, P <0.05) and also between CCO and HSP60 (r =0.679, P <0.05).
Conclusion: HS preconditioning ameliorates the burn-induced acute gastric mucosal lesion and has a protective role to gastric mucosal mitochondria. The role of HS preconditioning on mitochondria is associated with the protection of the activity of antioxidase and CCO by HSP60 and 70.