| Ischemia - reperfusion ( I/R) injury commonly occured during thrombolytic therapy for myocardial infarction, restoration of blood flow after cardioplegic arrest in cardiovascular surgery, and heart transplantation. It was a complicated pathophysiological process, involving in calcium overload, free radical production, metabolic abnormalities, and inflammatory reaction, etc. Along with development of modern molecular biology, expression and regulation of gene in I/R myocardium were focused on nuclear transcription factor - KB ( NF -KB) and inhibitory KB ( IKB ).NF - KB belongs to a rel/NF - KB protein family and found primarily in immune, inflammation and cellar defenses, which played very important roles in regulating multiple immediate - early gene expressions. The reasons were probably related to impact on the process of inflammatory reaction, cellular apoptosis and necrosis, ischemic preconditioning and ventricular remodeling, etc, especially involving in positive and negative feedback, and cross - regulation in NF - KB activation. However, the exact mechanism was unclear, thus, it is necessary to further explore the molecular mechanisms of NF - KB activation in myocardial I/R injury.Tumor necrosis factor - a ( TNF - a) , an important inflammatory cytokine, was regulated by NF - KB and counteracted on NF - KB activation. Improper activation of NF - KB could induce excessive inflam-matory responses and injury. Therefore, modulation of NF - KB activation might dedicate a new target in alleviation of myocardium I/R injury.Our previous studies had proved that Peucedanum Praeruptorum Dunn ( BQ) , isolated from a traditional Chinese medicine " Bai - Hua Qian - Hu" , had cardioprotective effects. And dl - praeruptorin A ( Pd - la) , a Ca + - influx blocker and K+ - channel opener relieved inflammatory reaction and apoptosis in I/R myocardium through inhibition of interleukin - 6 (IL - 6 ) and Fas, bax, bcl - 2 protein expression. However, the effects of BQ and Pd - la on NF - KB activation and TNF - a expression in I/R myocardium had not been investigated. In the present study, the influences of BQ and Pd - la on these two factors were firstly observed. It probably brought further comprehension to the mechanisms of BQ and Pd -Ia in I/R myocardium and offered a new target of therapy for ischemic disease.Methodssixty -four Wistar rats (200 -400 g, Grade II, Certificate No [2000] 015) of both sexes supplied by Laboratory Animal Center of China Medical University were divided randomly into nine groups; sham; solvent; diltiazem 1.2 mol - L-1; BQ ( ( g L-1 )0. 1, 0. 5, 1.0]; Pd-Ia [(( mol 1 )0.2, 1.0, 3.0]. The rat was killed and the heart was transferred to the perfusion apparatus. After equilibrium , global normothermic ischemia was initiated for 10 - min and re-flowed for 30 - min. myocardial contraction ( MC) , heart rate ( HR) and coronary flow (CF) were examined before ischemia and 10, 20 and 30 min after reperfusion, respectively. Meanwhile, perfusing fluidwas collected to detect the activity of lactate dehydrogenase ( LDH) and creatine Kinase (CK). Left ventricles were preserved for protein isolation and wax section preparation at the end of experiment. All data was expressed as mean ?SD. One - way ANOVA analysis was used by SPSS software to assess statistical significance between drug groups and various related control groups. P <0. 05 was considered to be significant.Results1. Effects on cardiohemodynamicsBQ dose - dependently declined MC, but P >0.05 ; HR was decreased slightly; BQ 0. 5 g L-1 increased CF from (6. 61 5. 78) % to (27.40 48.16) % (P<0.01, vs sham).Pd-Ia (0.2 mol - L-1, 1.0 mol L-1, 3.0 mol L-1) dose - dependently decreased MC (P <0. 05, vs solvent) , and the mean inhibitory rates were (32.82 19.76) %, (54.66 19.56) % and (57. 10 29. 97) % , respectively. Also Pd-Ia reduced HR slightly. Pd - Ia expressed a dual action to CF, it increased CF at lower dose (0.2 mol L-1) , but decreased it at highter dose (3.0 mol L-1 ), (P<0.05, vs solve...
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