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Objective: Myocardial ischemia / reperfusion experimental model, observed diosgenin pharmacological preconditioning on myocardial ischemia-reperfusion injury physiology, infarct size, morphological changes and biochemical aspects discussed on myocardial protective effect, provide a reference for clinical application. Methods: Male Wistar rats were randomly divided into IR group and IPC group, the high-dose group (D_H), low-dose group (DL). IR group d gavage 0.9% saline 10mL/kg DH group every d to gavage Dioscin 300mg/kg and DL groups per d orally 150mg/kg, 7d. 24h after the last administration, IPC group perform IPC program that 5min ischemia followed by 5min reperfusion, repeated three times, and the remaining three groups exclusion after 30min, copy myocardial ischemia-reperfusion injury model, the left anterior descending coronary artery ligation branch, ischemia 30 min / reperfusion 120 min. Continuous monitoring of standard II lead ECG recording heart rate, blood pressure, ST-segment changes, as well as the period of ischemia arrhythmia; determination before ligation ligation 30min and reperfusion 2h plasma creatine kinase (creatinekinase, CK) activity, nitric oxide ( nitric oxide, NO) content. Reperfusion 2h end line trypan blue, TTC staining; myocardial tissue malondialdehyde (malondialdehyde, MDA) content, superoxide dismutase (superoxide dismutase, SOD) activity was measured in each group were randomly selected three rat left ventricle HE staining, quantitative and qualitative determination of myocardial necrosis; rats left ventricular infarction extract myocardial tissue RNA using semi-quantitative RT-PCR method for determination of Mn-SOD content. Results: I diosgenin on myocardial ischemia-reperfusion injury physiology incidence of arrhythmia: IR group (81.25%), IPC group (0%), D_H group (0%) and D_L group (12.5% ) compared with IR group, a significant difference (P <0.01), no significant difference in the between D_H, and D_L group. The VPC occur time and duration: IR group (3.82 ± 1.33min; 21.69 ± 4.79min), the IPC group (12.97 ± 2.82min; 10??? .84 Min), D_H groups (14.07 ± 3.29min; 8.76 ± 2.99min) , D_L group (10.34 ± 2.73min; 11.64 ± 3.69min), compared with IR group a significant difference (P <0.01), D_H and D_L group difference was not significant. The the VT occurrence time and duration: IR group (6.81 ± 1.84min; 17.26 ± 2.97min), the IPC (16.74 ± 2.97min; 9.43 ± 2.14min) D_H group (18.88 ± 1.76min; 7.54 ± 1.79min) D_L group (14.44 ± 2.77min; 10.39 ± 2.94min), compared with the IR group, a significant difference (P <0.01), D_H and D_L no significant differences. Period of ischemia and 30 minutes with ST-segment elevation: IR group (0.472 ± 0.082mV), IPC group (0.331 ± 0.048mV), D_H group (0.305 ± 0.032 mV), D_L group (0.370 ± 0.027 mV), and IR group significant difference (P <0.01), D_H and D_L group difference was not significant. Ⅱ. Diosgenin on myocardial ischemia-reperfusion injury after myocardial infarct size and morphology affect the IR group myocardial infarct size (48.59 ± 9.84%); IPC group was significantly reduced myocardial necrosis range (24.03 ± 5.12%); D_H group significantly reduced myocardial necrosis range (21.48 ± 2.72%); D_L group significantly reduced myocardial necrosis range (23.86 ± 5.65%), with the IR group comparison there is a significant difference (P <0.01), D_H and D_L group differences without significantly with sex. III diosgenin on myocardial ischemia reperfusion injury biochemical and Mn-SOD expression in plasma CK activity: IR group reperfusion period plasma CK increased significantly during reperfusion (122.55 ± 18.11U / L); reduced in IPC group degree of elevated plasma CK activity (98.15 ± 12.5U / L); D_H significantly reduced the degree of elevated plasma CK activity during reperfusion (92.37 ± 13.96U / L); D_L group was significantly lower during reperfusion plasma CK activity liter high degree of (99.25 ± 15.38 U / L), compared with IR group, a significant difference (P <0.01), D_H and D_L group, the difference was not significant. Plasma NO content: the IR group ischemia NO vigor before ligation obviously decreased (23.53 ± 5.81U / L) and reperfusion increase of NO (31.03 ± 5.86 U / L); IPC group reduce ischemia during plasma NO vitality NO increased during reperfusion reduced the extent of (30.54 ± 4.80U / L) enhanced the degree of (40.95 ± 7.98 U / L), compared with IR significant difference (P <0.05); D_H group to reduce ischemia during plasma NO activity was reduced NO increased the extent of the degree of (35.48 ± 6.88U / L) enhanced during reperfusion (44.70 ± 11.07 U / L), a significant difference (P <0.01); D_L group to reduce ischemia during plasma NO activity was reduced compared with IR the degree of (32.74 ± 9.83U / L) enhanced the degree of increase of NO during reperfusion (41.59 ± 9.34 U / L), a significant difference (P <0.05) compared with IR. Myocardial MDA content: IR MDA content (2.87 ± 0.89 nmol / mg): IPC group MDA content decreased (1.62 ± 0.69 nmol / mg?? The H group MDA content decreased significantly (1.44 ± 0.30nmol/mg); D_L group MDA content was significantly decreased (1.58 ± 0.48 nmol / mg), and IR group comparison there is a significant difference (P <0.01), D_H and D_L group differences without significantly with sex. myocardial tissue SOD vitality: IR group SOD vitality (T-SOD 158.73 ± 16.21 U / prog; Mn-SOD 60.69 ± 19.29U/prog); the IPC group SOD activity increased (T.SOD183.95 ± 26.26U/prog; Mn-SOD, 105.19 ± 30.62 U / prog); D_H group SOD activity was significantly higher (T-SOD215.74 ± 18.31U/prog; Mn-SOD 116.46 ± 19.56U/prog); the DE group SOD activity was significantly increased (T-SOD 198.19 ± 29.09U/prog; Mn-SOD108.61 ± 28.88U/prog ), of Mn-SOD expression was significantly enhanced with IR comparison there is a significant difference (P <0.01), D_H and D_L differences without significantly with sex. myocardial Mn-of SOD expression: IR group (0.45 ± 0.12); in IPC group (0.68 ± 0.09) ; D_H group (0.76 ± 0.11); D_L group (0.71 ± 0.12), with the IR group comparison there is a significant difference (P <0.01), D_H and D_L group differences without significantly with sex. conclusion: diosgenin reduce the period of ischemia room occurrence of arrhythmias, reduce ischemia / reperfusion myocardial necrosis, enhanced myocardial Mn-SOD mRNA expression, plasma NO content, lower CK activity during reperfusion, decreased MDA content, enhanced myocardial tissue Mn-SOD activity play a cardioprotective effect its mechanisms and antioxidant free radical damage and protect the vascular endothelium.
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