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2017 ; 18
(10
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
High Endogenous Accumulation of ?-3 Polyunsaturated Fatty Acids Protect against
Ischemia-Reperfusion Renal Injury through AMPK-Mediated Autophagy in Fat-1 Mice
#MMPMID28974016
Gwon DH
; Hwang TW
; Ro JY
; Kang YJ
; Jeong JY
; Kim DK
; Lim K
; Kim DW
; Choi DE
; Kim JJ
Int J Mol Sci
2017[Sep]; 18
(10
): ä PMID28974016
show ga
Regulated autophagy is involved in the repair of renal ischemia-reperfusion
injury (IRI). Fat-1 transgenic mice produce ?3-Polyunsaturated fatty acids
(?3-PUFAs) from ?6-Polyunsaturated fatty acids (?6-PUFAs) without a dietary
?3-PUFAs supplement, leading to a high accumulation of omega-3 in various
tissues. ?3-PUFAs show protective effects against various renal injuries and it
has recently been reported that ?3-PUFAs regulate autophagy. We assessed whether
?3-PUFAs attenuated IR-induced acute kidney injury (AKI) and evaluated its
associated mechanisms. C57Bl/6 background fat-1 mice and wild-type mice (wt) were
divided into four groups: wt sham (n = 10), fat-1 sham (n = 10), wt IRI
(reperfusion 35 min after clamping both the renal artery and vein; n = 15), and
fat-1 IRI (n = 15). Kidneys and blood were harvested 24 h after IRI and renal
histological and molecular data were collected. The kidneys of fat-1 mice showed
better renal cell survival, renal function, and pathological damage than those of
wt mice after IRI. In addition, fat-1 mice showed less oxidative stress and
autophagy impairment; greater amounts of microtubule-associated protein
1A/1B-light chain 3 (LC3)-II, Beclin-1, and Atg7; lower amounts of p62; and,
higher levels of renal cathepsin D and ATP6E than wt kidneys. They also showed
more adenosine monophosphate-activated protein kinase (AMPK) activation, which
resulted in the inhibition of phosphorylation of the mammalian target of
rapamycin (mTOR). Collectively, ?3-PUFAs in fat-1 mice contributed to AMPK
mediated autophagy activation, leading to a renoprotective response.