OBJECTIVE: To investigate the protective effect of total flavonoid of Herba Pyrolae (TFHP) on acute myocardial ischemic injury induced by isoproterenol in rats and the primary mechanisms. METHODS: Acute myocardial ischemic models were established by i. s. of isoproterenol. ECG of the rats were recorded, activities of creatine phosphokinase (CK), lactate dehydrogenase (LDH) and the superoxide dismutase (SOD), and the levels of malondialdehyde (MDA), NO and FFA in rat serum were determined, heart index were measured and histopathological changes of myocardium were observed. RESULTS: In comparison with model group, TFHP raised the height of T wave, reduced CK, LDH activities and FFA levels in serum, decreased heart index and relieved myocardial ischemic injury. The primary study of its mechanism showed that TFHP decreased MDA level, increased SOD activity and NO levels in the rat serum. CONCLUSION: TFHP has protective effect on acute myocardial ischemic injury possibly via antioxidation and increasing the release and production of NO.
OBJECTIVE: To investigate the protective effect of total flavonoid of Herba Pyrolae (TFHP) on acute myocardial ischemic injury induced by isoproterenol in rats and the primary mechanisms. METHODS: Acute myocardial ischemic models were established by i. s. of isoproterenol. ECG of the rats were recorded, activities of creatine phosphokinase (CK), lactate dehydrogenase (LDH) and the superoxide dismutase (SOD), and the levels of malondialdehyde (MDA), NO and FFA in rat serum were determined, heart index were measured and histopathological changes of myocardium were observed. RESULTS: In comparison with model group, TFHP raised the height of T wave, reduced CK, LDH activities and FFA levels in serum, decreased heart index and relieved myocardial ischemic injury. The primary study of its mechanism showed that TFHP decreased MDA level, increased SOD activity and NO levels in the rat serum. CONCLUSION:TFHP has protective effect on acute myocardial ischemic injury possibly via antioxidation and increasing the release and production of NO.