Mechanism of the protective effects of N-acetylcysteine on the heart of brain-dead Ba-Ma miniature pigs.

BACKGROUND

Severe stress response induced by brain death leads to a marked increase in the expression of inflammatory cytokines regulated by nuclear factor-kappaB (NF-kappaB). N-acetylcysteine may inhibit activation of the NF-kappaB pathway. This study examined the expression of NF-kappaB in the hearts of brain-dead Ba-Ma miniature pigs and the protection potential of N-acetylcysteine.

METHODS

Ba-Ma miniature pigs were randomized into 3 groups: control group (Group C), N-acetylcysteine-free group (Group B), and N-acetylcysteine treatment group (Group N). At 6, 12, and 24 hours after the initial brain death, serum cardiac troponin-T (cTnT), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 were examined. Heart tissue was taken 24 hours after the initial brain death. Structural changes of the heart and the expression of NF-kappaB were analyzed.

RESULTS

At 6 hours after the initial brain death, serum levels of cTnT, TNF-alpha, IL-1beta, and IL-6 in Groups B and N began to increase. Levels in Group B increased more dramatically than in Group N. At 24 hours, cardiocyte damage was documented, but the damage in Group N was less severe than that in Group B. The expression of NF-kappaB in Groups B and N increased, and expression in Group B increased more sharply than in Group N.

CONCLUSIONS

N-acetylcysteine can alleviate both structural and functional injury of the heart during brain death, which might be related to the inhibition of NF-kappaB expression and decreasing release of inflammatory mediators.