Jin Jin-Lan, Lv Rong-Gui, Guo Jian, Liu Xi-Hong, Liang Yan-Wen, Wei Jian-Rui, Wang Lexin
Central Intensive Care Unit, Guangzhou Red Cross Hospital, Medical College of Jinan University, Guangzhou 510220, Guangdong, China.
Department of Cardiology, Guangzhou Red Cross Hospital, Medical College of Jinan University, Guangzhou 510220, Guangdong, China.
Heart Lung Circ. 2016 Oct;25(10):1007-12. doi: 10.1016/j.hlc.2015.11.005. Epub 2015 Nov 28.
To investigate the effects of inhibition of NF-κB activation on left ventricular (LV) remodelling in a rat model of myocardial infarction (MI).
The acute MI model was established by ligation of left anterior descending coronary artery. Pyrrolidine dithiocarbamate (PDTC) (20mg/kg, Qd) was administered intraperitoneally to inhibit NF-κB activation. Eight weeks later, the cardiac structure and LV ejection fraction were assessed with echocardiography. The rat body, heart, and LV weights were measured to calculate LV mass indices. Activation of NF-κB in non-infarcted myocardium was detected by a TransAM NF-κB p65 Transcription Factor Assay Kit. Cardiac collagen volume fraction was evaluated by Masson staining.
Eight weeks after the MI model was established, the LV posterior wall thickness in PDTC and MI group was 1.75±0.07mm and 1.85±0.07mm respectively (p<0.05). The LV mass index in the PDTC group (2.53±0.09) was lower than in the MI group (2.65±0.08, p<0.05). The LVEF in the PDTC group (63.89%±4.21%) was higher than in the MI group (42.73%±8.94%, p<0.05). The interstitial collagen deposition in the non-infarcted myocardium in the PDTC group was less than in the MI group (7.25%±1.88% vs. 10.09%±2.19%, p<0.05).
Inhibition of activation of NF-κB may result in improvement of myocardial remodelling after myocardial infarction, which is possibly attributable to reduced collagen deposition in non-infarcted areas.
研究抑制核因子κB(NF-κB)激活对心肌梗死(MI)大鼠模型左心室(LV)重构的影响。
通过结扎左冠状动脉前降支建立急性MI模型。腹腔注射吡咯烷二硫代氨基甲酸盐(PDTC)(20mg/kg,每日一次)以抑制NF-κB激活。8周后,用超声心动图评估心脏结构和左心室射血分数。测量大鼠体重、心脏重量和左心室重量以计算左心室质量指数。用TransAM NF-κB p65转录因子检测试剂盒检测非梗死心肌中NF-κB的激活情况。通过Masson染色评估心脏胶原容积分数。
MI模型建立8周后,PDTC组和MI组的左心室后壁厚度分别为1.75±0.07mm和1.85±0.07mm(p<0.05)。PDTC组的左心室质量指数(2.53±0.09)低于MI组(2.65±0.08,p<0.05)。PDTC组的左心室射血分数(63.89%±4.21%)高于MI组(42.73%±8.94%,p<0.05)。PDTC组非梗死心肌的间质胶原沉积少于MI组(7.25%±1.88%对10.09%±2.19%,p<0.05)。
抑制NF-κB激活可能会改善心肌梗死后的心肌重构,这可能归因于非梗死区域胶原沉积减少。