[Sesamin Preconditioning Attenuates Myocardial Ischemia Reperfusion Injury in Rats Through Activation of Akt/eNOS Signaling Pathway].

Objective: To investigate the protective effect of sesamin on myocardial ischemia reperfusion injury in rats, and to study the possible mechanism.

Methods: 50 SD rats were randomly divided into control group, sham operated group, model group, high-dose sesamin group( 160 mg / kg) and low-dose sesamin group( 80 mg / kg),with 10 rats in each group. Rats in sesamin groups were administered intragastrically with sesamin for 7 d. Then all rats except those in sham operated group were subjected to myocardial ischemia-myocardial ischemia reperfusion injury model by coronary artery ligation for 40 min and subsequent reperfusion for 120 min. Serum cardiac troponin Ⅰ( c TnⅠ) and lactate dehydrogenase( LDH),levels of total antioxidant capacity( TAOC) and nitric oxide( NO) in serum and myocardial tissues,Caspase-3 activity in myocardial tissues were detected by colorimetric assay. Cardiomyocyte apoptosis was evaluated by TUNEL assay. Phosphorylation level of endothelial nitric oxide synthase( eNOS) and Protein kinase B( Akt), protein expression of superoxide dismutase( SOD) in cardiac tissue were determined by Western blot.

Results: Pretreatment with sesamin significantly ameliorated myocardial injury in rats which induced myocardial ischemia and reperfusion injury by reduced levels of serum c TnⅠand LDH( P <0. 05 or P < 0. 01). Supplementation with sesamin resulted in a significant increasing of total antioxidant capacity and NO level in serum and myocardial tissues and cardiomyocyte apoptosis( P < 0. 05 or P < 0. 01),and remarkable decrease the Caspase-3 activity in myocardial tissues and cardiomyocyte apoptosis( P < 0. 05 or P < 0. 01). Sesamin significantly up-regulated the protein expression of SOD in cardiac tissues, and the levels of phosphorylated eNOS and Akt increased notably( P < 0. 05 or P < 0. 01).

Conclusion: Pretreatment with sesamin effectively ameliorated myocardial ischemia reperfusion injury in rats, and the mechanism might be related to enhancing its antioxidant capacity and the activation of Akt / eNOS signaling pathway and subsequent increase of NO synthesis and suppression of cardiac myocyte apoptosis.