Mechanism of crush syndrome on myocardial cell injury in rats / 中国医师杂志

ABSTRACT

Objective:To investigate the mechanism of crush syndrome (CS) induced by crush injury on myocardial cells in rats.Methods:Thirty two male Sprague Dawley (SD) rats were randomly divided into control group, CS-0 group, CS-12 group and CS-24 group with 8 rats in each group. CS model was made by self-made extruder and perfused with 4% paraformaldehyde for 0, 12 and 24 h. The morphological changes of myocardial tissue were observed by hematoxylin staining. The apoptosis of cardiomyocytes was detected by terminal dexynucleotide transferase-mediated nick end labeling (TUNEL). The levels and activities of malondialdehyde (MDA), superoxide dismutase (SOD), lactose dehydrogenase (LDH), interleukin-6 (IL-6), interleukin-1 β (IL-1 β), tumor necrosis factor-α (TNF- α) in myocardial homogenate were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of Caspase-3, Bax, Bcl-2 and necrosis factor-κB (NF-κ B) were detected by Western blot.Results:Compared with the control group, the myocardial tissue of CS model group had different degrees of morphological damage; compared with the control group, the apoptosis rate, Caspase-3 and Bax protein expression levels of CS-0 group, CS-12 group and CS-24 group were significantly increased ( P<0.05), and the expression level of Bcl-2 protein was significantly decreased ( P<0.05); compared with the control group, the levels of MDA, LDH, IL-6, IL-1β, TNF-α and p65 protein phosphorylation in the myocardial homogenate of CS-0 group, CS-12 group and CS-24 group were significantly increased ( P<0.05), and SOD activity was significantly decreased ( P<0.05). Conclusions:CS may inhibit oxidative stress and induce inflammatory reaction by activating NF-κ B pathway, thus damaging myocardial cells in rats.