Protective Effect And Possible Mechanism Of Astragalus Injection In Ischemia Reperfusion Cardiocytes

OBJECTIVE Astragalus "survival" signaling attenuates apoptosis. We therefore examined the effects of astragalus on reperfusion injury cardial myocytes and assessed the role of p42/p44 MAPK signaling in astragalus-induced protection. METHODS Using a blood-perfused, parabiotic, Langendorff rabbit model, hearts underwent 45 minutes of normothermic ischemia protected with Astragalus or not, and 60 minutes of reperfusion. Hemodynamic parameter and myocardial enzyme leak were compared. Further studies were conducted on cultured cells. Rat ventricular myocytes were subjected to hypoxia 4h and reoxygenation 2h. Astragalus was applied to cells before or during ischaemia/reoxygenation and the extent of cell death and myocardial enzyme was determined. RESULTS When intact hearts received astragalus during ischamia, hemodynamic parameter, CK release and ischamic size were better, compared with control group (p<0.01). In cells, incubation with Astragalus before or during reoxygenation attenuated the extent of cell damage and also reduced the numbers of apoptotic cells. Reduction of apoptosis was decreased by PD98059, an inhibitor of p42/p44 MAPK activation. Astragalus activated p42/p44 MAPK transiently in normoxic myocytes. CONCLUSIONS This studies show that astraglus attenuates cardiac myocytes injury during reperfusion and the mechanism perhapa involves p42/44 MAPK activation.