Pterostilbene attenuates the inflammatory reaction induced by ischemia/reperfusion in rat heart.

Abstract

The role of pterostilbene (Pte) in inflammation induced by ischemia/reperfusion is not well understood. The aim of this study was to investigate whether Pte modulates neutrophil accumulation and the induction of tumor necrosis factor-α (TNF-α) in an ischemia/reperfusion (I/R)-injured rat heart model. Rats were randomly exposed to a sham operation, myocardial ischemia/reperfusion (MI/R) alone, MI/R+Pte, MI/R+Pte+L-NAME and MI/R+Pte+ (methylene blue) MB. The results demonstrated that compared with MI/R, Pte reduced the area of myocardial infarction, the levels of myocardial myeloperoxidase, serum creatinine kinase and lactate dehydrogenase, and the production of serum and myocardial TNF-α. These Pte-induced effects were eliminated by the administration of L-NAME, a nitric oxide (NO) synthase inhibitor, and MB, a cyclic guanosine monophosphate (cGMP) inhibitor. In conclusion, Pte produces cardioprotective and anti-inflammatory effects. These effects may be associated with an increase in NO production, the inhibition of neutrophil accumulation, and induction of TNF-α and cGMP signaling pathways in myocardium subjected to MI/R.