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Basic science: Experiment research
e0229 Inhibition of NF-κB attenuates post-infarct left ventricular rupture and remodelling in aged mice by ribozyme gene transfer with adeno-associated virus serotypes 9
  1. Xiang Yang,
  2. Ma Yitong,
  3. Yang Yining,
  4. Chen Bangdang,
  5. Liu Fen,
  6. Gao Xia,
  7. Du Lei
  1. Department of Cardiovascular Medicine, The First Affiliated Hospital Xinjiang Medical University, Urumqi, China

Abstract

Objective Using intravenous injection of adeno-associated virus serotypes 9 carring ribozyme gene (AAV9-R65), we examined whether inhibition NF-κB would prevent post-infarct left ventricular rupture and remodelling in aged mice.

Methods and results Old (18-month-old) C57BL/6 male mice were given AAV9-R65 by tail vein injection 16 days before operation (MI+R65). Myocardial infarction was induced by ligation of the left coronary artery in MI+R65 group and myocardial infarction (MI) group mice. NF-κB activity was inhibited in MI+R65 mice. Inhibition of NF-κB reduced cardiac rupture in MI+R65 group (15.2% vs 32.8%, p=0.018). Echocardiographic measurements revealed that diameter of LV was significantly decreased, and ventricular wall thickness, fraction shortening were significantly increased in MI+R65 mice compared with MI mice (p<0.05). MMP-9 and TNF-α were decreased in MI+R65 group (p<0.05). And collagen was also decreased in MI+R65 group (p<0.05). But there were no changes of IL-1β in MI+R65 group.

Conclusions Cardiac rupture and remodelling were attenuated in aged mice by ribozyme gene transfer with adeno-associated virus serotypes 9. It maybe caused by decreased collagen as the result of decreased MMP-9, TNF-α which proved that NF-κB signal pathway may be associated with cardiac rupture and remodelling in aged mice.

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