Ligustrazine attenuates myocardial ischemia reperfusion injury in rats by activating the phosphatidylinositol 3-kinase/Akt pathway.

To the Editor: Coronary revascularization has been well-established as the most effective treatment of limiting the eventual infarct size for coronary artery diseases. However, reperfusion can elicit a number of adverse reactions that may limit its beneficial actions. Although reduction of ischemia reperfusion (IR) injury through the use of antioxidant therapy, calcium-channel blockers, sodium-hydrogen exchange inhibitors, and antiinflammatory drugs has previously been attempted in many studies, few agents are clinically available for protecting the heart from IR injury [1]. Activation of the pro-survival kinase-signaling cascade phosphatidylinositol 3-kinase (PI3K) /Akt at the time of reperfusion promotes cell survival and recruits the anti-apoptotic pathway during reperfusion [2]. Experimental studies have indicated that the intervention and ischemia preconditioning of some pharmacological agents can recruit the PI3K/Akt pathway and confer powerful cardioprotection [3]. It has been proposed that pharmacological targeting of the Akt pathway may potentially diminish IR injury [4]. In a recent study [5], we reported that ligustrazine (2,3,5,6-tetramethylpyrazine,TMP), an alkaloid extracted from Ligusricum wallichii Franchat (Apiaceae), has cardioprotective effects against myocardial IR injury through limitation of infarct size and reduction of apoptosis. In this article, we further investigated whether the cardioprotective effect of TMP was dose-dependent through observing the ultrastructure, enzyme level, and oxidative stress of the myocardium and whether the PI3K/Akt signal pathway was involved in the cardioprotective effect of TMP using Western blot analysis.