Post-TTM Rebound Pyrexia after Ischemia-Reperfusion Injury Results in Sterile Inflammation and Apoptosis in Cardiomyocytes

Figure 3

(a) TNF-α expression was suppressed by OGD (6 h). OGD/R-induced damage leads to a significant increase in TNF-α expression relative to normoxia control in the early reperfusion phase (8 h), which was significantly higher in the cooled than in the noncooled group. During late reperfusion (31 and 41 h), however, the noncooled OGD/R-injured group stayed significantly elevated, whereas the cooled group showed no such effect. Further warming to pyrexia induced TNF-α expression in OGD/R-injured groups irrespective of previous temperature management. (b) IL-6 expression was suppressed by OGD (6 h), and hypothermia temporarily attenuated pyrexia-induced IL-6 expression in OGD/R-injured cardiomyocytes (41 h). (c) Pyrexia increased IL-1β expression in noncooled OGD/R-injured cardiomyocytes that was not attenuated by hypothermia (53 h). (d) SOCS-3 expression was significantly inhibited by OGD (6 h) and increased during late reperfusion (31 h) in the noncooled OGD/R-injured groups. Warming to pyrexia significantly induced SOCS-3 expression in both cooled and noncooled OGD/R-injured cardiomyocytes and was briefly attenuated by hypothermia (41 h). Data from 3 to 5 independent experiments is presented as . and as compared to normoxia control at 37°C (normalized to 1).

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