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Objective: Previous studies have shown t hat allitridum can protect myocardium from ischemia/reperfusion (I/R) injury, bu t whether allitridum had the effect of anti-apoptosis is unclear. The aim of th is study was to investigate whether allitridum had the effects of pharmacologica l preconditioning and decreasing myocardium apoptosis after ischemic insult. Methods: Pentobarbital sodium-anesthetized Sprague-Dawley (SD) rats underwent 30 min of left anterior descending (LAD) coronary occlusion foll owed by 120 min of reperfusion. Thirty-six rats were divided into three groups randomly: Control group, I/R group and allitridum (G) group. The control and I/R groups with saline, G group with allitridum were administrated 24 h before oper ation. Control group underwent only sham operation; the other two groups underwe nt I/R operation. Infarcted size (IS/AAR %) was measured in I/R and G groups. Ma londialdehyde (MDA), Creatine kinase isoenzyme-MB (CK-MB ), Superoxide dismuta se (SOD)and the apoptosis index (AI) by TUNEL staining were measured in each gro up. In addition, DNA fragmentation by agarose gel electrophoresis was conducted on DNA isolated from these groups. Results: Allitridum p retreatm ent decreased the infarcted size compared with I/R group in IS/ AAR%[(21.85±1. 49)% vs. ( 44.65±4.65)%, P<0.01], CK-MB [(986.40±94.01) vs. (2044.2 5±1 07.28) U/L, P<0.01] and MDA [(3.26±0.35) vs. (4.96±0.46) nmol/mg pro, P<0.01], and SOD level in G group was higher than that of I/R group [(140 .20±12.89)vs. (73.16±11.22) U/mg pro, P<0.01]. AI of I/R group was highe r than that of G group [(13.99±3.05)% vs. (6.97±1.23)%, P<0.01], which was consistent with that in DNA fragmentation by agarose gel electrophoresis. Conclusion: This study indicated that allitridum had the effect of protecting myocardium against I/R injury and decreasing infarcted zone. The e ffect was probably through decreasing myocardium apoptosis in I/R injury.
Objective: Previous studies have shown that all hatch can protect myocardium from ischemia / reperfusion (I / R) injury, bu t whether allitridum had the effect of anti-apoptosis is unclear. The aim of th is study was to investigate whether allitridum had the effects of pharmacological l preconditioning and reducing myocardium apoptosis after ischemic insult. Methods: Pentobarbital sodium-anesthetized Sprague-Dawley (SD) rats underwent 30 min of left anterior descending (LAD) coronary occlusion foll owed by 120 min of reperfusion. Thirty-six rats The control and I / R groups with saline, G group with allitridum were administrated 24 h before oper ation. Control group underwent only sham operation; The two groups underwe nt I / R operation. Infarcted size (IS / AAR%) was measured in I / R and G groups. Ma londialdehyde (MDA), Creatine kinase isoenzyme-MB (CK-MB), Superoxide dismuta se ( SOD) and the apoptosis index (AI) by TUNEL staining were measured in each gro up. In addition, DNA fragmentation by agarose gel electrophoresis was conducted on DNA isolated from these groups. Results: Allitridum p retreatm ent decreased the infarcted size compared with I / R group The results showed that the ratio of CK-MB [(986.40 ± 94.01) vs. (2044.2 ± 5 07.28) U / L) in IS / AAR% [(21.85 ± 1.49)% vs (44.65 ± 4.65)%, P <0.01] P <0.01] and MDA [(3.26 ± 0.35) vs. (4.96 ± 0.46) nmol / mg pro, P <0.01] and SOD level in G group was higher than that of I / R group [(140 .20 ± (73.16 ± 11.22) U / mg pro, P <0.01]. AI of I / R group was highe r than that of G group [(13.99 ± 3.05)% vs. (6.97 ± 1.23)%, P <0.01], which was consistent with that in DNA fragmentation by agarose gel electrophoresis. Conclusion: This study indicated that allitridum had the effect of Protect myocardium against I / R injury and decreasing infarcted zone. The e ffect was likely through reducing myocardium apoptosis in I / R injury.