Effect of dl-3n-butylphthalide on sympathetic remodeling at infarct border zone in rats with myocardial infarction

Abstract

Objective To investigate the effect of dl-3n-Butylphthalide (NBP) on cardiac function and sympathetic remodeling in rats with myocardial infarction (MI). Methods Totally 50 male SD rats were randomly divided into 3 groups: Sham-operated (sham) group (n=10), myocardial infraction (MI) group (n=20) and MI with NBP group (n=20). A rat myocardial infarction model was established by ligating anterior descending branch of coronary artery. Rats in MI with NBP group were received the gavage treatment with NBP. Cardiac function was evaluated by hemodynamic detection at 7 day post-MI. Cardiac tissues were stained with hematoxylin and eosin as well as Masson trichrome. The distribution and density of growth associated protein-43- (GAP-43) and tyrosine hydroxytase- (TH) positive nerve at infarction border zone were detected by immunohistochemistry. The activation of nuclear factor-κB (NF-κB) signaling pathway was detected by western blot analysis. Results 8 rats died in MI group, in which 2 rats died within 24h. 7 rats died in MI with NBP group, and in which 3 rats died within 24 h. The left ventricular end-diastolic pressure (LVEDP) and left ventricular end-systolic pressure (LVESP) were (7.81±2.46) mmHg (1 mmHg=0.133 kPa) and (103.32±10.59) mmHg, (18.93±3.17) mmHg and (136.44±13.62) mmHg, (16.56±4.82) mmHg and (112.83±16.97) mmHg in sham group, MI group and MI with NBP group respectively. There were no significant differences in + dP/dt and - dP/dt between MI group and MI with NBP group (both P>0.05). Compared with sham group, the collagen volume fraction at infarct border zone was increased in MI group (P<0.05), but was reduced in MI with NBP group as compared to the MI group (P<0.05). The densities of GAP-43- and TH- positive nerves at infarct border zone were increased in MI group as compared with sham group, and reduced in MI with NBP group as compared with MI group (both P<0.05). NBP could reduced p-IKBα protein expression and increase IKBα protein expression in rats with MI. Conclusions NBP may improve the sympathetic remodeling after MI via the inhibition of NF-κB signaling pathway. Key words: Myocardial infarction; Apigenin; Parasympathetic nervous system