1.Expression of heat shock protein 70 in gastric mucosa of rats during the early stage after severe scald injury and the effect of insulin
Shengyong LONG ; Jun LIU ; Rouhong DING ; Zhiyong WENG ; Bin HAN ; Zhenghua CHEN
Journal of Chinese Physician 2011;13(5):630-633,637
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.