Sophocarpine administration preserves myocardial function from ischemia-reperfusion in rats via NF-κB inactivation.

BACKGROUND

Sophora alopecuroides L. (the clinical usefulness of compound Kudouzi injection) has been used mainly for the treatment of fever, inflammation, edema and pain. Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Sophocarpine injection (called the Kangke injection) has been demonstrated to have significant antivirus effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in clinical.

OBJECTIVE

The present study was to evaluate the protective effect of sophocarpine on the inhibition of NF-kappaB (NF-κB) and effect on inflammatory markers during myocardial ischemia-reperfusion (I/R) injury in rat.

METHODS

Myocardial I/R injury was induced by the occlusion of left anterior descending coronary artery for 30 min followed by reperfusion for 2 h. 2 h after reperfusion was established, the hemodynamics and infarct size were examined. Blood samples were collected for biochemical analysis. Expression of NF-κB and mitogen-activated protein kinases (MAPKs) in ischemic myocardial tissue were assayed by western blot.

RESULTS

Administration of sophocarpine significantly improved cardiac function and reduced infarct size in I/R rat heart in vivo. Furthermore, sophocarpine ameliorated the contents of inflammatory mediators (tumor necrosis factor-alpha, TNF-α; interleukin-6, IL-6; IL-10), neutrophil infiltration and myeloperoxidase (MPO) activity. Interestingly, sophocarpine also significantly inhibited translocation of NF-κB, which was associated with attenuated phosphorylations of p38 and c-Jun NH2-terminal protein kinase (JNK).

CONCLUSIONS

Inflammatory mediators, infiltration of neutrophil, and MPO were ameliorated via down-regulation of JNK and p38, and inactivation of NF-κB. This might be one of the important mechanisms of sophocarpine that protected myocardial injury from I/R.