Aim This thesis addresses the cardioprotective effects of Panax notoginsenoside Rb1 on angiotensinⅡ-induced hypertrophy of neonatal rat myocytes against hypoxia-reoxygenation injury. The results demonstrate the potential prospects of Panax notoginsenoside Rb1 in clinical application.Method Cultured cardiomyocytes were used in the experiments. The inducing medicine results in myocardial hypertrophy. This was then applied to perform the treatment of hypoxia/reoxygenation (H/R) injury (similar to the ischemic and reperfusion (IR) injury in animal experiments). This study focuses on investigating the protective effects of Panax notoginsenoside Rb1.Hypertrophied cardiomyocytes of cultured neonatal Wistar rats were induced by AngⅡ0.01-10μmol·L-1 Rb1. The H/R injury model was established after treatment with Rb1 for 48h.The confocal microscopy LSM510 was applied to scan the cell surface area (CSA). We used the Coomassie Brilliant Blue Protein Detection Kit to measure the total protein content (TP) in myocytes. The detailed content of LDH, NO, NOS and MDA can be seen from the instruction. MTT colorimetry was used to measue the survival rate of the cells, and flow cytpmetry using PI stain was applied to analyze the apoptosis of cardiomyocytes.Result In comparison with the H/R group, the CSA of Rb1 group is down by 41.56% (P<0.01); the total protein content is up by 43.37% (P<0.01); the LDH is down by 59.20% (P<0.01); it has a 2.67-fold (P<0.01) increase in the activity of NO and has a 2.44-fold (P<0.01) increase in the activity of NOS; the MDA is down by 72.03%(P<0.01); it has a 2.28-fold (P<0.01) increase in the survival rate of cell; and the apoptosis rate is donw by 85.29% (P<0.01).Conclusion To sum up, Panax notoginsenoside Rb1 preconditioning has protective effects on the H/R injury, caused by AngⅡ, to the cultured neonatal Wistar rats. It can significantly reduce this injury. The results show that its protective mechanisms assit in inhibiting the cellular apoptosis, reducing lipid peroxidation and the release of LDH, and enhancing the activity of NO and NOS. |