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2015 ; 2015
(ä): 362158
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Nephroprotective Effects of Polydatin against Ischemia/Reperfusion Injury: A Role
for the PI3K/Akt Signal Pathway
#MMPMID26576221
Liu HB
; Meng QH
; Huang C
; Wang JB
; Liu XW
Oxid Med Cell Longev
2015[]; 2015
(ä): 362158
PMID26576221
show ga
Oxidative stress and inflammation are involved in the pathogenesis in renal
ischemia/reperfusion (I/R) injury. It has been demonstrated that polydatin
processed the antioxidative, anti-inflammatory, and nephroprotective properties.
However, whether it has beneficial effects and the possible mechanisms on renal
I/R injury remain unclear. In our present study I/R models were simulated both in
vitro and in vivo. Compared with vehicle control, the administration of polydatin
significantly improved the renal function, accelerated the mitogenic response and
reduced cell apoptosis in renal I/R injury models, strongly suppressed the
I/R-induced upregulation of the expression of tumor necrosis factor-?,
interleukin-1?, cyclooxygenase-2, inducible nitric oxide synthase, prostaglandin
E-2, and nitric oxide levels, and dramatically decreased contents of
malondialdehyde, but it increased the activity of superoxide dismutase,
glutathione transferase, glutathione peroxidase and catalase, and the level of
glutathione. Further investigation showed that polydatin upregulated the
phosphorylation of Akt in kidneys of I/R injury dose-dependently. However, all
beneficial effects of polydatin mentioned above were counteracted when we
inhibited PI3K/Akt pathway with its specific inhibitor, wortmannin. Taken
together, the present findings provide the first evidence demonstrating that PD
exhibited prominent nephroprotective effects against renal I/R injury by
antioxidative stress and inflammation through PI3-K/Akt-dependent molecular
mechanisms.
|Animals
[MESH]
|Antioxidants/metabolism
[MESH]
|Cyclooxygenase 2/genetics/metabolism
[MESH]
|Disease Models, Animal
[MESH]
|Glucosides/chemistry/*pharmacology
[MESH]
|Interleukin-1beta/genetics/metabolism
[MESH]
|Kidney/metabolism/pathology
[MESH]
|Male
[MESH]
|Mice
[MESH]
|Mice, Inbred BALB C
[MESH]
|Nitric Oxide Synthase Type II/genetics/metabolism
[MESH]