Background: To investigate the effect of N -acetylcysteine (NAC) on oxidative stress and inflammation induced by acute fluctuations in blood glucose and the potential mechanism.
Methods : Cannulated Wistar rats (n=6/group) were infused intravenously for 48 h with (1) saline (control), (2) 50% glucose intermittently (IHG), (3) 50% glucose continuously (PHG), (4) IHG plus NAC, or (5) PHG plus NAC. Levels of superoxide dismutase (SOD), nitric oxide (NO), nuclear factor-κB (NF-κB), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF) in cardiac tissues were analyzed. We also evaluated apoptosis in the myocardium using a terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay.
Results : The IHG group had higher levels of oxidative and inflammatory markers in the myocardium than the PHG and control groups. Co-infusion with NAC prevented the elevation in inflammatory markers and NF-κB activity in the IHG + NAC and PHG + NAC groups. Apoptosis of myocardial cells was observed in the IHG group but was abolished by co-administration of NAC.
Conclusions : Acute fluctuations in blood glucose levels induced more severe oxidative stress, inflammation and apoptosis in the myocardium than persistently high blood glucose levels. The antioxidant NAC may prevent apoptosis of myocardial cells caused by fluctuations in blood glucose levels in vivo , most likely because of its antioxidative and anti-inflammatory properties.