Objective: The aim of the present study was to investigate whether pterostilbene could modulate the TLR4/NF-kappa B signaling, reduce neutrophil accumulation and TNF-alpha induction in an ischemia/reperfusion injured rat heart model. Materials and Methods: Rats were randomly exposed to sham operation, myocardial ischemia and reperfusion (MI/R), MI/R + pterostilbene, MI/R + pterostilbene + L-NAME. And myocardial infarct size, apoptosis, TLR4 expression, NF-kappa B expression, MPO level and TNF-alpha level were detected. Results: The results demonstrated that after MI/R, the expressions of myocardial TLR4, NF-kappa B and caspase-3 increased significantly in ischemia area. Compared with MI/R, pterostilbene significantly attenuated the expressions of TLR4, NF-kappa B and caspase-3. In addition, it also reduced myeloperoxidase (MPO) levels, both serum and myocardial TNF-alpha production, myocardial infarct sizes (INF/AAR%) and myocardial apoptosis induced by MI/R. All the effects of pterostilbene were abolished by L-NAME, a nitric oxide synthase inhibitor. Conclusion: These data provide evidence that pterostilbene inhibits TLR4/NF-kappa B signaling and apoptosis in the rat heart subjected to MI/R, which is associated with NO production.

OBJECTIVE:The aim of the present study was to investigate whether pterostilbene could modulate the TLR4/NF-κB signaling, reduce neutrophil accumulation and TNF-α induction in an ischemia/reperfusion injured rat heart model.MATERIALS AND METHODS:Rats were randomly exposed to sham operation, myocardial ischemia and reperfusion (MI/R), MI/R + pterostilbene, MI/R + pterostilbene + L-NAME. And myocardial infarct size, apoptosis, TLR4 expression, NF-κB expression, MPO level and TNF-α level were detected.RESULTS:The results demonstrated that after MI/R, the expressions of myocardial TLR4, NF-κB and caspase-3 increased significantly in ischemia area. Compared with MI/R, pterostilbene significantly attenuated the expressions of TLR4, NF-κB and caspase-3. In addition, it also reduced myeloperoxidase (MPO) levels, both serum and myocardial TNF-α production, myocardial infarct sizes (INF/AAR%) and myocardial apoptosis induced by MI/R. All the effects of pterostilbene were abolished by L-NAME, a nitric oxide synthase inhibitor.CONCLUSION:These data provide evidence that pterostilbene inhibits TLR4/NF-κB signaling and apoptosis in the rat heart subjected to MI/R, which is associated with NO production.