OBJECTIVE: To study the direct effect of hawthorn leaf procyanidins on cardiomyocytes subjected to ischemia-reperfusion injury and elucidate their therapeutic mechanism on ischemic heart diseases. METHOD: Cultured cardiomyocytes of neonatal rats were subjected to anoxia-reoxia injury which simulated the ischemia-reperfusion injury in vivo, and hawthorn leaf procyanidins were applied. The therapeutic effect was valued by LDH leakage and MTT test. For a further mechanism study, contents of MDA and activities of SOD in cardiomyocytes were measured. RESULT: Hawthorn leaf procyanidins in 24-60 mg x L(-1) significantly and dose-dependently inhibited LDH leakage (compared with the model group, all P<0.01 ) and cell viability decrease (compared with model group, 24-48 mg x L(-1) groups all P<0.05; 60 mg x L(-1) group, P<0.01) in cardiomyocytes induced by anoxia-reoxia injury. Furthermore, hawthorn leaf procyanidins in 24-60 mg x L(-1) significantly inhibited the increase of MDA content (compared with the model group, all P<0.01) and the decreased of SOD activity (compared with the model group, 24 mg x L(-1) group, P<0.05; other groups all P<0.01) in cardiomyocytes undergoing anoxia-reoxia injury. CONCLUSION: Hawthorn leaf procyanidins have a significant therapeutic effect on the simulated ischemia-reperfusion injury of cultured neonatal rat cardiomyocytes, which may relate to their anti-oxidation effects. And the direct protective effect of hawthorn leaf procyanidins on cardiomyocytes subjected to ischemia-reperfusion injury may be one of the key mechanisms of its therapeutic effect on ischemic heart diseases.
OBJECTIVE: To study the direct effect of hawthorn leaf procyanidins on cardiomyocytes subjected to ischemia-reperfusion injury and elucidate their therapeutic mechanism on ischemic heart diseases. METHOD: Cultured cardiomyocytes of neonatal rats were subjected to anoxia-reoxia injury which simulated the ischemia-reperfusion injury in vivo, and hawthorn leaf procyanidins were applied. The therapeutic effect was valued by LDH leakage and MTT test. For a further mechanism study, contents of MDA and activities of SOD in cardiomyocytes were measured. RESULT: Hawthorn leaf procyanidins in 24-60 mg x L(-1) significantly and dose-dependently inhibited LDH leakage (compared with the model group, all P<0.01 ) and cell viability decrease (compared with model group, 24-48 mg x L(-1) groups all P<0.05; 60 mg x L(-1) group, P<0.01) in cardiomyocytes induced by anoxia-reoxia injury. Furthermore, hawthorn leaf procyanidins in 24-60 mg x L(-1) significantly inhibited the increase of MDA content (compared with the model group, all P<0.01) and the decreased of SOD activity (compared with the model group, 24 mg x L(-1) group, P<0.05; other groups all P<0.01) in cardiomyocytes undergoing anoxia-reoxia injury. CONCLUSION: Hawthorn leaf procyanidins have a significant therapeutic effect on the simulated ischemia-reperfusion injury of cultured neonatal rat cardiomyocytes, which may relate to their anti-oxidation effects. And the direct protective effect of hawthorn leaf procyanidins on cardiomyocytes subjected to ischemia-reperfusion injury may be one of the key mechanisms of its therapeutic effect on ischemic heart diseases.