虾青素抑制NF-κB的激活减轻大鼠心肌梗死后的交感神经重构的研究

Astaxanthin delays sympathetic remodeling after myocardial infarct ion by inhibiting NF-κB activation

目的探讨虾青素对心肌梗死后的交感神经重构的影响以及可能的作用机制。方法心肌梗死组和虾青素组大鼠结扎冠状动脉前降支制作心肌梗死模型;假手术组开胸后剪开心包腔,不结扎冠状动脉。虾青素组按100 mg/(kg·d)的剂量于术前1日开始灌胃,1次·d-1;心肌梗死对照组和假手术组灌胃等量无菌蒸馏水。28 d后用HE染色观察细胞形态,采用蛋白免疫印迹法检测心肌梗死周边NF-κB核移位、p-CX43蛋白的表达。采用免疫组化方法检测心肌梗死周边神经生长因子(NGF)、生长相关蛋白43(GAP43)、酪氨酸羟化酶(TH)的分布。结果与心肌梗死组相比,虾青素抑制了NF-κB核移位,p-CX43蛋白水平表达增多,虾青素组GAP-43与TH阳性的密度及NGF的含量明显减少。结论虾青素可减轻心肌梗死周边的交感神经重构,可能是通过抑制NF-κB的激活。

Objective To investigate the effect of astaxanthin on the sympathetic remodeling at the infarcted border zone （IBZ） after myocardial infarction （MI）, and the possible mechanism. Methods The MI model was made in the astaxanthin （ASX） group and the MI group by ligation of the coronary artery. The sham-operated group rats were per- formed pericardiotomy, but not ligation. The rats were dosed with astaxanthin [the ASX group, 100 mg/（kg ·d）] or distilled water （the sham-operated group and the MI group） by lavaging daily 1 d pre-operation. At 28 d post-operation, Western blot was used to examine the expression of nuclear transcription factor （NF）-κB translocation and p-CX43 at the IBZ. At the same time, heart pathology in the rats was observed with HE staining; tyrosine hydroxylase （TH）, nerve growth factor （NGF） and growth associated protein 43 （GAP-43） were analysed by immunohistochemistry. Results Compared with the MI group, treatment with astaxanthin can inhibited NF-κB translocation, and increased p-CX43 expression. Astaxanthin decreased the density of positive staining for GAP-43 and TH, and the levels of NGF. Conclu- sion Astaxanthin can delay the sympathetic remodeling at the IBZ after MI, likely through the inhibition of NF-κB