ABSTRACT
OBJECTIVE: To investigate the effect of intensive insulin treatment, in the protection of myocardiocytes against apoptosis in severely scalded rats and its underlying mechanism. METHODS: Eighteen Sprague-Dawley (SD) rats were randomly divided into three groups (6/each) to receive: sham surgery, burn damage (on the back of the animals, degreeIII, to 30% of total body surface area), and burn damage+intensive insulin treatment. Tissue samples were collected from the left ventricle 6 hours after infliction of the burn damage for the examination of myocardial cell apoptosis [by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining] and the expression of apoptosis-related molecules caspase-3, Bax, and Bcl-2 (by immuno-histochemistry and Western blotting). RESULTS: In comparison with the animals in sham treated group, the myocardiocyte apoptosis rate in animals in burn damage only group increased significantly [(13.1 ± 3.4)% vs. (0.6 ± 0.4)%, P < 0.01]. The expression of caspase-3 and Bax both significantly increased while the level of Bcl-2 expression significantly decreased (immuno-histochemistry caspase-3: 13.72 ± 4.13 vs. 1.36 ± 0.95, Bax: 29.64 ± 5.42 vs. 2.24 ± 1.04, Bcl-2: 3.39 ± 1.52 vs. 8.01 ± 2.56; Western blotting caspase-3: 5.72 ± 2.13 vs. 1, Bax: 4.64 ± 1.42 vs. 1, Bcl-2: 0.69 ± 0.42 vs. 1, all P < 0.01). The animals received intensive insulin treatment showed significantly less myocardiocyte apoptosis [(6.7 ± 1.8)% vs. (13.1 ± 3.4)%, P < 0.01], significantly lower expression in caspase-3, Bax, and significantly higher level of Bcl-2 expression as compared to the animals in burn damage only group (immuno-histochemistry caspase-3: 8.88 ± 3.36 vs. 13.72 ± 4.13, Bax: 14.43 ± 3.69 vs. 29.64 ± 5.42, Bcl-2: 8.61 ± 3.72 vs. 3.39 ± 1.52; Western blotting caspase-3: 2.18 ± 0.86 vs. 5.72 ± 2.13, Bax: 2.87 ± 1.35 vs. 4.64 ± 1.42, Bcl-2: 3.57 ± 1.70 vs. 0.69 ± 0.42, P < 0.05 or P < 0.01). CONCLUSION: Intensive insulin therapy may protect myocardiocytes against apoptosis in severely burned animals through the regulation of the expression of apoptosis-related molecules caspase-3, Bax and Bcl-2.
