ObjectiveTo investigate the correlation between tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), phospholipase A2 (PLA2) and myocardial cell function disorders in severe chest-abdominal injury patients. MethodsEighty-two subjects with severe chest-abdominal injury were collected from January 2009 to June 2012, of whom the trauma index were all above or equal to 17 points. As the rescue and treatment were in progress, the patients were examined for their creatine kinase-MB (CK-MB), cardiac troponin T (cTnT), TNF-α, IL-6, and PLA2 for correlation analysis. Another 82 subjects undergoing physical examination during the same time were chosen as the controls, who were again divided into myocardial cell function control group with 46 subjects and injury factors control group with 36 subjects. ResultsFor the myocardial cell function control group, CK-MB was (8.13±3.64) U/L, and cTnT was (26.71±11.58) pg/mL; for the injury group, those two indexes were respectively (158.74±31.59) U/L and (496.25±58.46) pg/mL. For the injury factors control group, TNF-α was (1.28±0.59) ng/mL, IL-6 was (63.93±41.49) ng/mL, and PLA2 was (7.47±5.27) ng/mL; for the injury group, those three indexes were respectively (36.41±18.09) ng/mL, (393.83±143.86) ng/mL, and (41.35±14.26) ng/mL. For severer chest-abdominal injury patients, all correlation factors between CK-MB and TNF-α, IL-6, PLA2 were above 0.911, and the factors between cTnT and TNF-α, IL-6, PLA2 were all above 0.912, and all correlations were positive. ConclusionTNF-α, IL-6 and PLA2 all participate in the process of acute myocardial cell function disorders in severe chest-abdominal injury patients. Early intervention of TNF-α, IL-6, and PLA2 may reduce myocardial cell damage, and improve patients' survival rate.
With the oxidative damage model established in rat myocardial cells by hydrogen peroxide (H2O2), the expression of myocardin and nuclear factor erythroid 2-related factor 2 (Nrf2) during oxidative damage and effect of myocardin on Nrf2 were preliminarily explored. The expression of the target gene was increased or decreased by transfection of plasmid DNA or shRNA, respectively. Cell proliferation was detected by sulforhodamine B (SRB) assay. The expression of myocardin mRNA and Nrf2 mRNA was detected by Real-time PCR, and their protein levels were detected by Western blot. The results showed that oxidative damage was induced by H2O2 with an optimized incubation condition of 200 μmol/L H2O2 for 24 hours. H2O2 inhibited expression of myocardin in mRNA and protein levels, and increased expression of Nrf2 in mRNA and protein levels. The overexpression of myocardin or the knockdown of Nrf2 significantly decreased cell viability compared with the control group, while the knockdown of myocardin or the overexpression of Nrf2 significantly increased cell viability. The overexpression of myocardin significantly down-regulated the expression of Nrf2 in mRNA and protein levels, while the knockdown of myocardin dramatically up-regulated the expression of Nrf2. Thus, it is deduced that myocardin may inhibit cell proliferation and Nrf2 may promote cell proliferation. Oxidative damage induced by H2O2 in rat myocardial cell might activate Nrf2-related signaling pathway through down-regulation of myocardin.