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everal studies have shown that omega-3 polyunsaturated fatty acids (PUFAs) diet can reduce kidney dysfunction following
transgenic mice produce abundant omega-3 PUFAs, resulting in balanced omega-6 : omega-3 ratio
in comparison to wild type (WT) mice. Therefore, the purpose of this study was to determine whether omega-3 PUFAs are
protective in AKI caused by ischemic injury using
To induce AKI, mice were subjected to renal ischemia-reperfusion injury (IRI). Animals were sacrificed at 24 hr and 72 hr
of post-reperfusion. After that, renal function and severity of renal injury were estimated.
BUN (blood urea nitrogen) and serum creatinine levels were decreased in
group at 24 hr post-IRI, although the
difference was not statistically significant. The levels were significantly decreased in
group compared to WT group at 72 hr
post-IRI. The difference in Kim-1 expression was not statistically significant due to intragroup variation, but the fold-increase in
Kim-1 expression in
group was less than that in WT group. Relatively more lesions were observed on
group than on
WT group at 24 hr post-IRI. However, at 72 hr post-IRI, more lesions were observed in WT than in the
infiltration was reduced at 72 hr in the
group as compared to the WT group.
This study demonstrates that omega-3 PUFAs exert a protective effect on ischemia-induced AKI. Long-term and high-dose
omega-3 supplements may preserve renal function and facilitate renal recovery following AKI
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