Effect of phenolic alkaloids from Menispermum dauricum on myocardial-cerebral ischemia-reperfusion injury in rabbits
Abstract
Aim: To explore the mechanism underlying the effect of phenolic alkaloids from Menispermum dauricum (PAMd) on simultaneous myocardial-cerebral ischemia-reperfusion injury in rabbits.
Methods: Both left anterior descending coronary artery and bilateral carotid arteries were occluded to induce myocardial-cerebral ischemia-reperfusion injury in rabbits. At 30 min after ischemia, the occlusion was removed and shed blood was rapidly reinfused. Two mL of blood was taken fr om femoral artery at 10 min before ischemia, 1, 10, and 30 min after ischemia, and 1, 10, 30, 60, 120, 180, and 240 min after reperfusion. Each rabbit was sacrificed at the end of reperfusion, and left ventricle, hippocampus, cortex, and cerebellum were taken out. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined.
Results: At 10 min after reperfusion, MDA content in serum was significantly higher and SOD activity was lower in ischemia-reperfusion (I-R) group than those of control group (P < 0.05). After administration of PAMd, MDA content was lower and SOD activity was higher in serum than those of I-R group (P < 0.05). Both MDA content and SOD activity in tissues had the similar results with those in serum.
Conclusion: PAMd could attenuate the injury induced by lipid peroxidation and enhance the activity of SOD, thus PAMd might play a protective role in simultaneous myocardial-cerebral ischemia-reperfusion injury.
Keywords:
Methods: Both left anterior descending coronary artery and bilateral carotid arteries were occluded to induce myocardial-cerebral ischemia-reperfusion injury in rabbits. At 30 min after ischemia, the occlusion was removed and shed blood was rapidly reinfused. Two mL of blood was taken fr om femoral artery at 10 min before ischemia, 1, 10, and 30 min after ischemia, and 1, 10, 30, 60, 120, 180, and 240 min after reperfusion. Each rabbit was sacrificed at the end of reperfusion, and left ventricle, hippocampus, cortex, and cerebellum were taken out. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined.
Results: At 10 min after reperfusion, MDA content in serum was significantly higher and SOD activity was lower in ischemia-reperfusion (I-R) group than those of control group (P < 0.05). After administration of PAMd, MDA content was lower and SOD activity was higher in serum than those of I-R group (P < 0.05). Both MDA content and SOD activity in tissues had the similar results with those in serum.
Conclusion: PAMd could attenuate the injury induced by lipid peroxidation and enhance the activity of SOD, thus PAMd might play a protective role in simultaneous myocardial-cerebral ischemia-reperfusion injury.