AimTo observe the effect of ligustrazine (tetramethylpyrazine,TMP) pretreatment on the inflammatory reaction of myocardial ischemia reperfusion (IR) injury in rats and to investigate the possible mechanism.MethodsForty-eight Sprague-Dawley rats were randomly divided into sham group, IR group, TMP pretreated group, NG-nitro-L-arginine methyl ester (L-NAME) group and TMP+L-NAME group.All hearts except those in the sham group were subjected to 35 min ischemia followed by 120 min reperfusion.The myocardial structure was observed under microscope.The activity of myocardial superoxide dismutase (SOD) and the content of malondialdehyde (MDA), myeloperoxidase (MPO), interleukin-1β(IL-1β) and nitric oxide (NO) were measured.The expression of endothelial nitric oxide synthase (eNOS) was detected by reverse transcription polymerase chain reaction and Western blot.ResultsCompared with the IR group, the myocardial tissues of the TMP group showed an increase in the SOD activity, a decrease in the MDA content, the MPO activity and the level of IL-1β.TMP pretreatment also increased the NO level and alleviated the neutrophil infiltration.The expression of eNOS mRNA and protein in the myocardium of rats in the TMP group increased significantly compared with that in the IR group.However, these effects could be significantly reversed by L-NAME which abolished the increase of NO production and eNOS mRNA and protein expression brought by TMP.ConclusionsPretreatment of TMP attenuated the inflammatory reaction of myocardial IR in rats.The cardioprotective mechanism of TMP may relate to its effects of increasing the expression of eNOS and the level of NO.