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2015 ; 8
(9
): 10653-61
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English Wikipedia
Fenofibrate, a PPAR? agonist, protect proximal tubular cells from albumin-bound
fatty acids induced apoptosis via the activation of NF-kB
#MMPMID26617775
Zuo N
; Zheng X
; Liu H
; Ma X
Int J Clin Exp Pathol
2015[]; 8
(9
): 10653-61
PMID26617775
show ga
Albumin-bound fatty acids is the main cause of renal damage, PPAR? is responsible
in the metabolism of fatty acids. Previous study found that PPAR? played a
protective role in fatty acids overload associated tubular injury. The aim of the
present study is to investigate whether fenofibrate, a PPAR? ligands, could
contribute to the renoprotective action in fatty acids overload proximal tubule
epithelial cells. We observed in HK-2 cells that fenofibrate significantly
inhibited fatty acids bound albumin (FA-BSA) induced up-regulation of MCP-1 and
IL-8. Treatment with fenofibrate attenuated renal oxidative stress induced by
FA-BSA as evidenced by decreased MDA level, increased SOD activity and catalase,
GPx-1 expression. FA-BSA induced apoptosis of HK-2 cells were also obviously
prevented by fenofibrate. Furthermore, fenofibrate significantly increased the
expression of PPAR? mRNA and protein in FA-BSA treated cells. Finally, the
activation of NF-kB induced by FA-BSA was markedly suppressed by fenofibrate.
Taken together, our study describes a renoprotective role of fenofibrate in fatty
acids associated tubular toxicity, and the transcriptional activation of PPAR?
and suppression of NF-kB were at least partially involved.