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Aim To explore the protective effect of pedunculoside (PE) on myocardial ischemia/reperfusion injury. Methods Rat model of acute myocardial ischemia reperfusion injury was prepared by ligating the left anterior descending coronary artery (LAD) of the heart for 30 min and reperfusion for 24 h, and the rats were randomly divided into seven groups (re = 10): sham group (Sham), acute myocardial ischemia reperfusion injury model group (M), captopril group (Capt), metoprolol group (MT), PE low, medium and high dosage groups (2. 5, 5 and 10 mg · kg
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OBJECTIVE: To explore the protective effect of glycyrrhetinic acid (GA) on myocardial ischemia/reperfusion injury. METHODS: Forty-eight healthy male SD rats were randomly and averagely divided into six groups: sham, control, and control with tanshinone ⅡA sodium injection, GA at low, median and high dosages. The rats were subjected to 30 min of ischemia, followed by 180 min reperfusion. The influence of GA on arrhythmic during reperfusion period was observed. At the end of reperfusion period, the concentrations of CK-MB and LDH in serum were measured with assay kits, and the myocardial infarct size was measured with colouring method. RESULTS: At the time of myocardial ischemia and reperfusion, the HR, MAP and PRI in any GA group were not significantly different compared with the control group. At the end of the reperfusion period, the myocardial infarct sizes were decreased significantly in median and high dosage GA groups compared with the control group (P < 0.05); the CK-MB concentration in serum in all the GA groups were much lower (P < 0.05); the LDH concentrations in serum were much lower in median and high dosage GA groups (P < 0.05). CONCLUSION: GA exerts protection against myocardial ischemia/reperfusion as shown by a significant reduction in infarct size and decreased concentrations of CK-MB and LDH in serum.
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Objective: To investigate the effect and mechanism of helix B surface peptide (HBSP) on myocardial ischemia reperfusion injury (MIRI) in experimental mice. Methods: The MIRI model was established by ligation of anterior descending coronary artery of the mice for 45 min and followed by corresponding treatment at 5 min before reperfusion. A total of 64 male ICR mice were randomly assigned to 4 group:①Sham group,②MIRI group, the mice received normal saline at 5 min before reperfusion,③HBSP group, MIRI mice received HBSP at 5 min before reperfusion and④HBSP+PD98059 group, MIRI mice received PD98059 (a speciifc blocker of ERK1/2) at 20 min before reperfusion and followed by HBSP at 5 min before reperfusion.n=16 in each group, all animals were treated for 2 hours. The area of myocardial infarction (MI) was detected by TTC-EB double staining method, the myocardial apoptosis rate was examined by TUNEL method, the levels of protein expression of ERK1/2 and phosphorylation of ERK1/2 were measured by Western blot analysis. Results: Compared with MIRI group, HBSP group presented decreased MI area, decreased myocardial apoptosis rate and increased phopsphorylation level of ERK1/2, allP Conclusion: HBSP may reduce the MI area via inhibiting myocardial apoptosis and therefore, protecting the experimental mice from MIRI; the mechanism might be related to the activation of ERK1/2 pathway.
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The present study was designed to evaluate the potency of antioxidant activity of sesame oil in-vitro model of myocardial ischemic reperfusion injury of rat. Sesame oil was administered orally to Wistar albino rats (180-200 g) in two different doses (n=6), by gastric gavage at a dose of 5 mL/kg b.w. (S1) and 10 mL/kg b.w (S2) daily for thirty days. Control and sesame oil treated rat hearts were subjected to invitro global ischemic reperfusion injury (5 min perfusion, 9 min noflow and 12 min reperfusion). A significant rise in TBARS and decrease of GSH, catalase, LDH, CK and AST occurred in the hearts subjected to in-vitro myocardial ischemic reperfusion injury indicate the myocardial damage through oxidative stress. In sesame oil treated rats there was a significant decrease in TBARS and significant increase in endogenous antioxidants and myocardial marker enzymes in all the groups. In 10 mL/kg treatment group, a significant rise in the levels of GSH, SOD and catalase were observed with marker enzymes, and it shows better recovery profile than the other groups subjected to in-vitro ischemic reperfusion injury. In histological studies, control rats which subjected to IR injury show extensive myocardial damage and all the treatment groups, shows preserved myocardium. The effect of sesame oil was compared with reference compound captopril. The present study demonstrates that the sesame oil treated by the dose 10 mL/kg augments endogenous antioxidant compounds of the rat heart and also prevents the myocardium from in-vitro model of myocardial ischemic reperfusion injury.
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Objective To investigate the correlation between caspase-3 and left ventricular function at different phases after ischemia-reperfusion. Methods Totally 36 wistar rats were randomly divided into Sham operation group and ischemia-reperfusion(IR)group. The rat ischemic cardiac region of IR group was taken after 1, 3, 6, 12 and 24-hour reperfusion followed to 30-minute ischemia and detected for the activity fragment of caspase-3 P20, the activity of caspase-3, myocardial apoptosis index, left ventricular function (LVF) and creatine kinase-MB (CK-MB) respectively. Results With reperfusion time prolonging, the activity fragment of caspase-3 P20 increased, the activity of caspase-3, myocardial apoptosis index, left ventricular function and CK-MB all changed. The activity fragment of caspase-3 P20 and CK-MB peaked at 6 h, and the activity of caspase-3 and myocardial apoptosis index at 12 h, and then maintained platform; LVSP and ?dp/dt_max increased while LVEDP decreased gradually with the reperfusion time prolonging. All indexes mentioned above of IR group had statistical significance as compared with that of Sham operation group(P