[Protection of heat shock preconditioning on acute gastric mucosal lesion in scalded rats and its mechanism].
OBJECTIVE
To observe the influence of heat shock preconditioning on the expressions of heat shock protein (HSP) 60 and HSP 70 and on the activities of cytochrome oxidase (CCO) and superoxide dismutase (SOD) in mitochondria in gastric mucosa of severely scalded rats, and to investigate its protective mechanism on acute gastric mucosal lesion in rats with severe scald.


METHODS
One hundred and forty-four Wistar rats were randomized into three groups, i. e. scald group ( n = 40, acute gastric mucosal lesion was made after scald, other 8 normal rats without scald were employed as blank control); HS group ( n =40, with heat shock preconditioning 20 h before scald), and other 8 rats preconditioned with heat shock but without scald were employed as experimental control I; actinomycin D group ( n = 40, with intraperitoneal injection of 0. 1 mg/kg actinomycin D 30 min before heat shock preconditioning and other treatment as HS group), and other 8 rats with merely actinomycin D injection were employed as experimental control II. Eight rats in each group were sacrificed and laparotomized at 3, 6, 12, 24 and 48 post-scald hours (PSH) , respectively to determine the index of gastric mucosal lesions (UI ) , the mRNA expressions of HSP70 and protein expression of HSP60 and HSP70, and the changes in the activities of SOD and CCO.


RESULTS
UI of the scalded rats increased as the time elapses, reaching the peak (12. 8 +/- 1.9) at 24 PSH. In addition, UI in HS group was significantly lower than that in scald group at each time-point except that at 3 PSH ( P < 0. 05 or 0. 01). The extent of gastric mucosal lesion in rats in actinomycin D group was obviously aggravated compared with that in scald and HS groups ( P <0. 05). The HSP70 mRNA expression in both scald and HS groups was increased at each time-points except for 48PBH, while that in actinomycin D group was increased at 24 PBH and 48PBH. The expressions of HSP70 and HSP60 were greatly increased in HS group compared with those in scald group ( P < 0. 05 or 0. 01) , while those in actinomycin D group were significantly inhibited ( P < 0. 05). The activities of CCO and SOD were gradually decreased in gastric mucosa in scald group, but it was greatly improved by HS preconditioning at 6, 12, 24 PSH ( P < 0. 05 or 0. 01).


CONCLUSIONS
Heat shock preconditioning is beneficial for the protection of acute gastric mucosal lesion of rats after severe scald, due to increase of HPS60 and HSP70 expression, and increase of CCO and SOD activities in mitochondria.
Zhang
Hong-yan
HY
Center of Burns , the First Affiliated Hospital of Nanchang University , Nanchang 330006 , PR China.
Lv
Nong-hua
NH
Xie
Yong
Y
Guo
Guang-hua
GH
Zhan
Jian-hua
JH
Chen
Jiang
J
D000818:Animals; D002056:Burns / Q000378:metabolism* / Q000473:pathology; D018834:Chaperonin 60 / Q000378:metabolism*; D003576:Electron Transport Complex IV / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D018869:Heat-Shock Response; D008297:Male; D024101:Mitochondrial Proteins / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
D018834:Chaperonin 60; D018840:HSP70 Heat-Shock Proteins; D024101:Mitochondrial Proteins; D013482:Superoxide Dismutase; D003576:Electron Transport Complex IV