Improvement of Left Ventricular Remodelling by Inhibition of NF-κB in a Rat Model of Myocardial Infarction

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• 作者：Jin-lan Jin ; MD^a ; Rong-gui Lv ; MD^b ; Jian Guo ; MD^c ; Xi-hong Liu ; MD^d ; Yan-wen Liang ; MD^a ; Jian-rui Wei ; MD^b ; ^{jianruiwei2014@163.com" class="auth_mail" title="E-mail the corresponding author} ; Lexin Wang ; FCSANZ^e ; ^{lwang@csu.edu.au" class="auth_mail" title="E-mail the corresponding author}
• 关键词：NF-κB ; Myocardial infarction ; Ventricular remodelling ; LV mass index ; LV ejection fraction
• 刊名：Heart, Lung and Circulation
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：25
• 期：10
• 页码：1007-1012
• 全文大小：646 K

文摘

To investigate the effects of inhibition of NF-κB activation on left ventricular (LV) remodelling in a rat model of myocardial infarction (MI).

Methods

The acute MI model was established by ligation of left anterior descending coronary artery. Pyrrolidine dithiocarbamate (PDTC) (20 mg/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.

Results

Eight weeks after the MI model was established, the LV posterior wall thickness in PDTC and MI group was 1.75 ± 0.07 mm and 1.85 ± 0.07 mm 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).

Conclusion

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.