| [Objective]To investigate the protective effects of ligustrazine injection or delayed ischemic preconditioning on rabbit myocardial ischemia-reperfusion injury, and approach its mechanism.[Methods]Using rabbit ischemia-reperfusion injury model in vivo, twenty-four adult health new Zealand rabbits were randomly devided into four groups of A B C D. group A( purely ischemia-reperfusion group): The chest was opened and left anterio coronary (LAD) was occluded by suture silk, the occlusion was maintained for 30 minutes and released with reperfusion for 120 minutes, group B (delayed ischemic preconditioning group) : 24 hours prior to LAD ischemia-reperfusion, two cycles of 5 minutes of myocardial ischemia followed by 10 minutes of myocardial reperfusion , after which the procedures were the same to group A.group C(ligustrazine injection preconditioning group): 24 hours prior to LAD ischemia-reperfusion, this group was administered intravenously with ligustrazine injection by the dose of 80mg/kg, after which the procedures were the same to group A.group D(sham operating group) : The chest was opened and left anterio coronary (LAD) was exposed with no futher procedures.The index variance of serous troponin I (cTnI) concentration superoxide dismutase (SOD) activity malondialdehyde (MDA) content were measured before ischemia 30 minutes after ischemia 30 minutes after reperfusion 120 minutes after reperfusion, also the Adenosine Triphosphate (ATP) content in the cardiac muscular tissues was detected , cadiocyte ultrastructural pathological changes were observed with light microscope and transmission electron microscope, the apoptosis index of cadiocyte was detected by terminal deoxynucleotide transferase-mediated deoxyuridine-biofin nick end labelling (TUNEL) method, the expression of Bcl-2 protein Bax protein heat shock protein 70 (HSP70) associated with apoptosis were analyzed by immunohistochemistry technique.[Results](DOn every time point after ischemia, the index of serous troponin I (cTnl) concentration and malondialdehyde (MDA) content in group A were obviously higher than that in group D (P<0.05), also, compared with group D, superoxide dismutase (SOD) activity were significantly lower on the time point of 30 minutes after reperfusion and 120 minutes after reperfusion in group A(P<0.05) , simultaneouly, cadiocyte ultrastructural pathologi-cal injury was aggravated in group A, the apoptosis index of cadiocyte and Bax protein expression were higher than that in group D (P<0.05), moreover, the Adenosine Tripho- sphate (ATP) of the cardiac muscular tissues and Bcl-2/Bax ratio were significantly lower in group A compared with group D (P<0.05) . (2) On every time point after ischemia, the index of serous troponin I (cTnl) concentration and malondialdehyde (MDA) content in group B and C were obviously lower than that in group A (P<0.05) , also, compared with group A, superoxide dismutase (SOD) activity were significantly higher on the time point of 30 minutes after reperfusion and 120 minutes after reperfusion in group B and C (P< 0.05 ) , simultaneouly , cadiocyte ultrastructural pathological injury was lessened in group B and C, the apoptosis index of cadiocyte and Bax protein expression were lower than that in group A (P<0.05) , moreover, the Adenosine Triphosphate (ATP) of the cardiac muscular tissues % Bcl-2 protein heat shock protein 70 (HSP70) and Bcl-2/Bax ratio were significantly higher in group B and C compared with group A(P<0.05).[Conclusion](1) The apoptosis phenomenon of cadiocyte was obviously aggravated after ischemia-reperfusion, which may be concerned with multiple factors: increased production of oxygen free radical; decreased vigor of antioxidase; impairment of mitochondria functional accompanied with drop in the Adenosine Triphosphate (ATP) of the cardiac muscular tissues; over expression of Bax protein accompanied with down regulation of Bcl-2/Bax ratio. (2)ligustrazine injection preconditioning can greatly inhibited the apoptosis of cadiocyte to exert its myocardial preservation effects, which is much similar to delayed ischemic preconditioning. (3) The myocardial preservation mechanisim in ligustrazine injection preconditioning was much similar to delayed ischemic preconditioning, and it may be related to following aspects: enhancement of the vigor of antioxidase after reper-fusion;improvement of energy metabolism in ischemic cadiocyte; lessened the impairment of mitochondria membrane structure and its function; up regulation the expression of Bcl-2 protenu heat shock protein 70 (HSP70) and Bcl-2/Bax ratio; down regulation the expression of Bax protein. |
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