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Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130
Myocardial ischemia-reperfusion (I/R) is a well-known
stimulus for acute inflammatory responses that promote cell death and impair pump function. Interleukin-10 (IL-10) is an endogenous, potent
anti-inflammatory cytokine. Recently, it has been proposed that IL-10
inhibits inducible nitric oxide synthase (iNOS) activity after
myocardial I/R and consequently exerts cardioprotective effects.
However, whether this actually occurs remains unclear. To test this
hypothesis, we utilized iNOS-deficient (
/), IL-10 /, and
IL-10/iNOS / mice to examine the potential mechanism of
IL-10-mediated cardioprotection after myocardial I/R. Wild-type, iNOS
/, IL-10 /, and IL-10/iNOS / mice were subjected to in vivo myocardial ischemia (30 min) and reperfusion (24 h).
Deficiency of iNOS alone did not significantly alter the extent of
myocardial necrosis compared with wild-type mice. We found that
deficiency of IL-10 resulted in a significantly (P < 0.05) larger infarct size than that in wild-type hearts. Interestingly,
deficiency of both IL-10 and iNOS yielded significantly
(P < 0.01) larger myocardial infarct sizes compared
with wild-type animals. Histological examination of myocardial tissue
samples revealed augmented neutrophil infiltration into the I/R
myocardium of IL-10 / and IL-10/iNOS / mice compared with
hearts of wild-type mice. These results demonstrate that 1)
deficiency of endogenous IL-10 exacerbates myocardial injury after I/R;
2) the cardioprotective effects of IL-10 are not dependent
on the presence or absence of iNOS; and 3) deficiency of
IL-10 enhances the infiltration of neutrophils into the myocardium
after I/R.
cytokines; nitric oxide; ischemia; myocardial injury; mouse
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