Combination of paeoniflorin and calycosin-7-glucoside alleviates ischaemic stroke injury via the PI3K/AKT signalling pathway.

CONTEXT: Paeoniflorin (PF) and calycosin-7-glucoside (CG, Paeonia lactiflora Pall. extract) have demonstrated protective effects in ischaemic stroke. OBJECTIVE: To investigate the synergistic effects of PF + CG on ischaemia/reperfusion injury in vivo and in vitro. MATERIALS AND METHODS: Male Sprague-Dawley rats were subjected to the middle cerebral artery occlusion/reperfusion (MCAO/R). After MCAO/R for 24 h, rats were randomly subdivided into 5 groups: sham, model (MCAO/R), study treatment (PF + CG, 40 + 20 mg/kg), LY294002 (20 mg/kg), and study treatment + LY294002. Males were given via intragastric administration; the duration of the in vivo experiment was 8 days. Neurologic deficits, cerebral infarction, brain edoema, and protein levels were assessed in vivo. Hippocampal neurons (HT22) were refreshed with glucose-free DMEM and placed in an anaerobic chamber for 8 h. Subsequently, HT22 cells were reoxygenated in a 37 °C incubator with 5% CO2 for 6 h. SOD, MDA, ROS, LDH and protein levels were measured in vitro. RESULTS: PF + CG significantly reduced neurobehavioral outcomes (21%), cerebral infarct volume (44%), brain edoema (1.6%) compared with the MCAO/R group. Moreover, PF + CG increased p-PI3K/PI3K (4.69%, 7.4%), p-AKT/AKT (6.25%, 60.6%) and Bcl-2/BAX (33%, 49%) expression in vivo and in vitro, and reduced GSK-3ß (10.5%, 9.6%) expression. In vitro, PF + CG suppressed apoptosis in HT22 cells and decreased ROS and MDA levels (20%, 50%, respectively). CONCLUSIONS: PF + CG showed a synergistic protective effect against ischaemic brain injury, potentially being a future treatment for ischaemic stroke.

[The effect of cyclovirobuxinum D on myocardial ischemia induced by coronary artery ligation in rats].

OBJECTIVES: To study the cardiac protection of Cyclovirobuxinum D (Cvb-D) in rats model. METHODS: The rats were subjected to left main coronary artery occlusion. The change about S-T segment, the area of myocardial injury (necrotic and ischemic areas), the amount of cardiac tissue malondialdehyde (MDA), the cardiactissue creatine phosphokinase (CPK) and the cardiac tissue superoxide dismutase (SOD) activation were measured. RESULTS: Compared to the model group, Cvb-D (1.1 mg/kg, 2.2 mg/kg dos-age) significantly reduce myocardial damage, reduce myocardial ischemia mode rats' sigma s-t of ECG, significantly reduce cardiac tissue CPK activation and MDA content, raise the cardiac tissue SOD activation in the rats with myocardial ischemia. CONCLUSION: Cvb-D is effective in treatment of myocardial ischemia in rats.