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Updated: May 17, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Protective effect of C5 shRNA on myocardial ischemia-reperfusion injury in rats
Kai Tang1, Yunjiu Cheng, Suhua Wu
1Department of Cardiology, First Affiliated Hospital, Sun Yat-Sen University, No. 58 Zhongshan Road II, Guangzhou, GD510080, China.
Insights
C5 shRNA preconditioning protects against myocardial ischemia-reperfusion (MI/R) injury by reducing inflammation and infarct size. This protective effect is linked to increased Akt phosphorylation, suggesting a role for the PI3K pathway.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Myocardial ischemia-reperfusion (MI/R) injury involves complement system activation.
- Terminal complement components, such as C5, are key mediators of MI/R injury.
Purpose of the Study:
- To investigate the protective effects of C5 shRNA preconditioning against MI/R injury.
- To elucidate the underlying mechanism of C5 shRNA's protective action.
Main Methods:
- Rats were preconditioned with C5 shRNA before inducing ischemia.
- Evaluated heart function, infarct size, histopathology, inflammatory cytokines, and troponin T levels.
- Assessed Akt phosphorylation using immunoblotting.
Main Results:
- C5 shRNA effectively inhibited C5 expression and attenuated MI/R injury.
- Preconditioning significantly reduced troponin T levels, pro-inflammatory cytokines, and infarct size by 40%.
- C5 shRNA preconditioning increased Akt phosphorylation.
Conclusions:
- C5 shRNA preconditioning demonstrates protective effects in a rat model of MI/R injury.
- The protective mechanism may involve the PI3K pathway and Akt phosphorylation.
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.