RESUMO
BACKGROUND: Reactive oxygen species-induced cell injury has been considered to be one of the main etiologic factors in ischemia-reperfusion injury (IRI). As a potential antioxidant agent, epigallocatechin gallate (EGCG) was examined in skeletal muscle of the rats after IRI with or without treatment. MATERIALS AND METHODS: Tourniquet application applied to the rats' hind limbs was selected as the appropriate IRI method. Animals were randomly distributed to one of the following groups: (1) sham control + SF (saline) (10 mg/kg/i.p.) (SC-SF), (2) IRI (4 + 2 h) + SF (10 mg/kg/i.p.) (IRI-SF), (3) IRI and EGCG (25 mg/kg/i.p.) (IRI-EG25), and (4) IRI and EGCG (50 mg/kg/i.p) (IRI-EG50). In another set of experiments with identical groups, the only difference was that the reperfusion period was 24 h. A number of different parameters relating to the damage seen in the skeletal muscles, lungs, kidneys, and liver and particular cytokines were measured by proper analytical methods. RESULTS: In comparison with the SC-SF group, IRI (4 + 2 h) induced an increase in the total oxidative status of skeletal muscle (10.17 ± 0.61 versus 15.74 ± 1.10) and blood creatine phosphokinase (CPK) (669.88 ± 50.23 versus 7202.38 ± 766.13) and lactate dehydrogenase levels (686.00 ± 67.48 versus 1343.00 ± 113.01). Although 25 mg/kg EGCG could not reverse these parameters to their normal levels, the higher dose of EGCG, that is, 50 mg/kg, was sufficient to prevent the increases seen in total oxidative status (8.55 ± 0.85) and CPK levels (4741.63 ± 339.40). In addition, reduced total antioxidant status of skeletal muscle in the IRI-SF group (0.50 ± 0.06) was elevated by the administration of EGCG (50 mg/kg) (0.85 ± 0.04). Regarding remote organ injury, only alanine transaminase (ALT) and aspartate transaminase (AST) levels were found to be increased, showing a slight damage in liver tissue. However, neither dose of EGCG was able to prevent this deleterious effect. As for cytokines (interleukin-1ß, IL-6, IL-8, tumor necrosis factor-α, and monocyte chemotactic protein-1), there were no differences between the study groups. In regard to long-term IRI (i.e., 4 + 24 h), statistically significantly elevated parameters in the IRI-SF group were as follows: CPK, lactate dehydrogenase, creatinine (Cr), and blood urea nitrogen. On the other hand, none of them were influenced by either dose of EGCG. According to the results, EGCG demonstrates a considerable protective effect toward IRI (4 + 2 h) of skeletal muscle. CONCLUSIONS: Although oxidative stress seems to play a significant role both in the pathogenesis of IRI and in the mechanism of action of EGCG, there is no evidence that inflammatory cytokines are, at least in our model, crucial mediators regarding the former events.