Effects Of Insulin Therapy On Apoptosis Of Smoke Inhalation Injury In Rat's Model

Objective Inhalation injury is one of main reasons of death in the early stage of burn patients, the mechanism of pathophysiology is closely related to apoptosis.Rats are as models in smoke inhalation damage, give rats subcutaneous insulin injections. In different time points respectively in the lung tissue measuring rats apoptosis index (AI), Bax and Bcl-2 expressions change, and rats lung tissue pathology changes. To investigate the influence of insulin therapy on cell apoptosis and the expressions of Bcl-2 and Bax on smoke inhalation injury in rats.Method Sixty-six clean level adult female SD rats are randomly divided into three groups, Normal control group 6, Inhaled damage group and Insulin therapy group are all 30, and Inhaled damage group and Insulin therapy group are divided into five subsections which are 2h,6h,12h,24h and 48h. The Insulin therapy group were subcutaneously injected 5U/kg insulin after inhalation injury, The Inhaled damage group were injected the same volume normal saline. Normal control group are not injured. And at 2h,6 h,12h,24h and 48h, blood glucose were detected, The pathological morphology changes in lungs were also examined under the optical microscope. The Transferase mediated nick end labeling TUNEL method was employed to measure lung tissue cell apoptosis, lmmunohistochemical method is used to detect anti-apoptotic protein Bcl-2 and Bax expression changes.Results 1 normal information after lung inhalation injury:Each group animals comparing weight was statistically significant. Rats through a special device smoke inhalation damage onset of shortness of rales or wheezes, heartbeat to accelerate and extract add indoor empty zone after five minutes break the performance gradually disappear, and the normal control group under the condition of static breath breathe smoothly, no shortness of breath and breathing difficulties and other symptoms2 the blood glueose in the three group:Inhaled damage rats, glucose, insulin increased marginally 2h treatment group reduce blood sugar, group compared with inhaled damage significant difference (P<0.05), insulin therapy with normal blood sugar control 6h significantly reduced, compare (P<0.05), the difference was statistically significant. Group compared with inhaled damage significantly reduced (P< 0.01).12h insulin therapy back to normal blood glucose, blood sugar is compared between three groups of all there is no significant difference (P> 0.05)3 the normal and pathological section of three group:The lungs of control group on visual inspection had normal color,normal congestion and edema. Saline group was found to have severe diffused and passive lung congestion.at 12h and 24h points. The insulin group were less edema and more fresh than the saline group. At 48h points the lung in the saline group were less edema than at the 12h points the insulin group were better than the saline group at the 48h points.4 Every rats groups at different time points cell apoptosis of lung tissue changes and Bcl-2 and Bax and expression changes:TUNEL dyeing results show that:in insulin therapy apoptosis index and inhaled damage group working with normal controls comparative differences in different time points were significantly statistical significance (P<0.01). Insulin therapy and inhaled damage group 2 h, in injury compared not statistically significant difference (P>0.05). After 6h different time points, insulin therapy group compared with inhaled damage, significantly reduced, and the apoptotic cells different time points are significantly higher than that of normal,24 hours each value can reach peak and differences are significant (P<0.01) Immunohistochemical results show:Bax and Bcl-2 and inhaled insulin treatment group and control group compared with normal damage group, each and between-group differences were significantly statistical significance (P<0.01). At Bcl-2 inhaled insulin therapy group and the damage to rise, and after 2h 24h maintained at high levels,2h 6h insulin therapy group compared with inhaled damage no obvious difference (P>0.05), after 6h between groups each and comparative significant difference (P<0.01). Bax at 2h insulin therapy and inhaled damage group (P>0.05) there,2h between groups after each and comparative differences are significant (P<0.01). After injury to inhaled insulin can directly promote early Bcl-2 transcription, inhibiting apoptosis Bax etc enhancers gene expression, cause Bcl-2 expression increases and the lower Bax expression, can effectively restrain early lung tissue after inhaled damage cell apoptosisConclusion After injury to inhaled insulin can directly promote early Bcl-2 protein expression, inhibiting apoptosis proteins such as Bax promoting. Bcl-2 expression causes the protein expression increases and Bax which the lower protein expression. Bcl-2/Bax increases. AI reduced. Thus can effectively restrain early lung tissue after inhaled damage cell apoptosis, reduce lung injury to protect lung tissue and purpose.