ABSTRACT
Aim To explore the effect of Shuanglong formula(SLF) on no-reflow in rats with myocardial is-chemia/reperfusion (I/R). Methods The rats were divided into five groups, namely, sham group, I/R group,SLF(5,2.5,1.25 g·kg-1)group. Treatment group received SLF decoction by gavage once a day for five days,while other groups were offered drinking wa-ter by gavage once a day for five days. The rats in I/R group and SLF-pretreated group were induced by iga-tion of left anterior descending coronary artery,and the rats were subjected to ischemia for 4h followed by reperfusion. Sham operation group did not undergo oc-clusion of the coronary artery. After 4 hours' reperfu-sion, real-time myocardial contrast echocardiography was used to monitor regional blood perfusion and cardi-ac functions. Blood was collected from the abdominal aorta and the serum was separated, and the levels of cTnT, CRP, CK and LDH were measured. The myo-cardial no-reflow area and infarction area were assessed by thioflavin S and nitrotetrazolium blue chloride, re-spectively. Results The SLF-pretreated group exhibi-ted significant reductions in the infarct area and no-re-flow area compared with I/R group(P <0.01 or P <0.05). In SLF-pretreated groups, β, A and A·β significantly increased as compared to those in I/R group. The LV anterior wall systolic and diastolic thicknesses (LVAW d/s) were significantly improved in SLF-pretreated group compared with those in I/R group. The LV internal diameter in systole (LVID s) and the LV volume in systole(LV s) were significantly reduced in SLF-pretreated group compared with those in I/R group. The EF, FS and SV were significantly improved in SLF-pretreated group compared with those in I/R group. The comparison between SLF-pretreated group and I/R group showed no significant difference in LDH, CK, cTnT, and CRP levels. Conclusion Shuanglong formula minimizes the sizes of myocardial infarct area and no-reflow area,improving regional my-ocardial blood flow and cardiac function.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of allicin on cardiac function and underlying mechanism in rat model of myocardial infarction (MI).</p><p><b>METHODS</b>Ninety-four Wistar rats were randomly assigned to 6 groups (n=14-16 per group): sham control group [underwent thoracotomy without left anterior descending (LAD) occlusion and only received an injection of the same amount of citrate buffer], MI control group (subjected to LAD occlusion and only received an injection of same amount of citrate buffer), positive control group (subjected to LAD occlusion and received an injection of diltiazem hydrochloride at the dose of 1.5 mg/kg), and MI + allicin groups (subjected to LAD occlusion and received an injection of allicin at the doses of 1.2, 1.8, and 3.6 mg/kg). All of the drugs were administered intraperitoneally daily for 21 days. The infarct area was measured by myocardial staining. Hematoxylin-eosin staining was used to observe the pathological changes. Cardiac function parameters were assessed by echocardiography. The myocardial apoptotic index was estimated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining. The expression of Bax and Bcl-2 were detected by quantificational real-time polymerase chain reaction and Western blot.</p><p><b>RESULTS</b>Treatment with allicin could attenuate the myocardial infarct area (P<0.05) and relieve the changes of the myocardium. The left ventricular anterior wall diastolic and systolic thicknesses were increased in the allicin-treated groups (P<0.05), while there was no signifificant difference in the left ventricular posterior wall diastolic and systolic thickness (P>0.05). The left ventricular internal diameter in systole, ejection fraction, fractional shortening, and stroke volume were dramatically elevated in allicin-treated rats (P<0.05). Allicin dose-dependently reduced creatine kinase and lactate dehydrogenase levels (P<0.05). The myocardial apoptotic index was also markedly lowered, and Bax expression was signifificantly decreased, whereas Bcl-2 expression exhibited an opposite trend in allicin-treated rats (P<0.05).</p><p><b>CONCLUSION</b>Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis, further improving cardiac function.</p>