CAJ | 학술논문

目的研究热休克蛋白(HSP70)在严重烫伤早期大鼠胃黏膜组织中动态表达变化及胰岛素和HSP70对严重烫伤早期大鼠胃黏膜组织的保护作用,探讨胰岛素促进HSP70表达的可能机制.方法采用大鼠烫伤模型,以免疫组织化学的方法和显微图像分析方法观察伤后3、6、12、24和48 h不同时相点胃黏膜组织中HSP70的表达情况及胃黏膜组织的病理形态学变化.结果治疗组除12 h时相点(9.40±1.52,P＝0.065)外其余不同时相点HSP70的表达水平分别高于烫伤组相同时相点HSP70的表达水平[(6.80±1.10,8.60±0.55,10.80±1.64,11.40±1.34),P＜0.05],治疗组各时相点胃黏膜损伤指数分别低于烫伤组相同时相点损伤指数[(4.05±0.36,11.97±1.15,20.98±2.83,13.92±0.94,1.60±0.55),P＜0.05].病理形态学变化显示对照组胃黏膜组织结构完整无损伤,烫伤早期SD大鼠胃黏膜组织损伤明显,治疗组SD大鼠胃黏膜组织损伤较烫伤组明显减轻.相关分析结果显示,HSP70与胃黏膜损伤指数、血糖之间呈正相关(r＝0.904,0.961,P＜0.01).结论胰岛素能够明显增强严重烫伤早期SD大鼠胃黏膜组织内HSP70的表达,促进胃黏膜组织HSP70的合成,可能是胰岛素保护胃黏膜组织的重要机制之一.
목적 연구열휴극단백(HSP70)재엄중탕상조기대서위점막조직중동태표체변화급이도소화HSP70대엄중탕상조기대서위점막조직적보호작용,탐토이도소촉진HSP70표체적가능궤제.방법 채용대서탕상모형,이면역조직화학적방법화현미도상분석방법관찰상후3、6、12、24화48 h불동시상점위점막조직중HSP70적표체정황급위점막조직적병리형태학변화.결과 치료조제12 h시상점(9.40±1.52,P＝0.065)외기여불동시상점HSP70적표체수평분별고우탕상조상동시상점HSP70적표체수평[(6.80±1.10,8.60±0.55,10.80±1.64,11.40±1.34),P＜0.05],치료조각시상점위점막손상지수분별저우탕상조상동시상점손상지수[(4.05±0.36,11.97±1.15,20.98±2.83,13.92±0.94,1.60±0.55),P＜0.05].병리형태학변화현시대조조위점막조직결구완정무손상,탕상조기SD대서위점막조직손상명현,치료조SD대서위점막조직손상교탕상조명현감경.상관분석결과현시,HSP70여위점막손상지수、혈당지간정정상관(r＝0.904,0.961,P＜0.01).결론 이도소능구명현증강엄중탕상조기SD대서위점막조직내HSP70적표체,촉진위점막조직HSP70적합성,가능시이도소보호위점막조직적중요궤제지일.
Objective To investigate the changes of the expressions of heat shock proteins 70 (HSP70) and insulin and HSP70 protect effect on the gastric mucosa of rats with scald injury, and explore the relationship between insulin and HSP70 . Methods With a model of 30 total body surface area (TBSA) full-thickness burned rats,the expression and distribution of HSP70 in the gastric mucosa was detected with immunohistochemical method and analyzed by a micro-image analysis system, and at the same time the pathological changes of the gastric mucosa tissue of each group were analyzed by Western blot and immunohistochemistry at the 3rd,6th,12th,24th and 48th hour postburn. Results The expression of HSP70 obviously decreased at the 48th hour post scald injury. The expression of HSP70 in the treatment group was significantly higher than that in the scalded group at most time points except the 12th(9.40±1.52,P＝0.065) hour and at equal parallel time［(6.80±1.10,8.60±0.55,10.80±1.64,11.40±1.34),P＜0.05］. The gastric mucosal injury index in the scalded group was significantly higher than that in the treatment group and at equal parallel time ［(4.05±0.36,11.97±1.15,20.98±2.83,13.92±0.94,1.60±0.55),P＜0.05］. In pathological observation, the control group manifested the intact gastric mucosal tissue formation, the scalded group showed obvious gastric mucosal tissue injury in the early phase of scald injury, while the treatment group showed less severe injury than the scald group. A positive correlationwas found in the gastric mucosal injury index and HSP70(r＝0.904,P＜0.01) and also between the serum glucose and HSP70(r＝0.961,P＜0.01).Conclusions Insulin increased the expression of HSP70 and decreased the gastric mucosal injury index in the gastric mucosal tissue of SD rats in the phase of scald injury. It may be one of the vital mechanisms of insulin protecting the gastric mucosal tissue.