Abstract
Myocardial ischemia and reperfusion (MI/R) injury is associated with activation of the complement system. Complement activation generates a series of bioactive substances, including early (C3a, C3b) and terminal (C5a, C5b-9) components. The terminal complement components are key mediators of MI/R injury. This study investigated whether C5 shRNA preconditioning has protective effects following MI/R injury and its potential mechanism. Rats were injected with C5 shRNA 2 days before induction of ischemia. The effects of C5 shRNA were evaluated by the assessment of heart function, infarct size, histopathology, inflammatory cytokine levels, and the plasma level of troponin T. Akt phosphorylation was assessed by immunoblotting. C5 shRNA efficiently inhibited C5 expression both in vitro and in vivo, and attenuated MI/R injury. C5 shRNA preconditioning significantly decreased the level of troponin T and the production of pro-inflammatory cytokine. The infarct size was decreased by 40% in C5 shRNA treated rats. Akt phosphorylation increased after C5 shRNA preconditioning. These results suggest that C5 shRNA preconditioning in rats has protective effects following MI/R injury; this may be partly effected by mediating the activation of the PI3K pathway and by phosphorylation of Akt.
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