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2017 ; 14
(1
): 447-452
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Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular
epithelial cells after hypoxia/reoxygenation
#MMPMID28672952
Chen H
; Huang RS
; Yu XX
; Ye Q
; Pan LL
; Shao GJ
; Pan J
Exp Ther Med
2017[Jul]; 14
(1
): 447-452
PMID28672952
show ga
The aim of the present study was to determine the effects of emodin, a natural
compound with antioxidant properties, on oxidative stress and apoptosis induced
by hypoxia/reoxygenation (H/R) in HK-2 human renal tubular cells. In HK-2 cells
subjected to H/R, it was observed that pre-treatment with emodin lead to an
increase in cellular viability and a reduction in the rate of apoptosis and the
B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 ratio. H/R alone caused a
significant increase in the levels of reactive oxygen species and malondialdehyde
(P<0.05) and a significant decrease in the activities of superoxide dismutase,
catalase and glutathione peroxidase (P<0.05), relative to normoxic cells. In
turn, parameters of oxidative stress were improved by emodin pre-treatment. In
addition, emodin pre-treatment significantly inhibited the phosphorylation of
extracellular signal-regulated protein kinase and c-Jun N-terminal kinase
mitogen-activated protein kinases (MAPKs) induced by H/R (P<0.05). These data
suggest that emodin may prevent H/R-induced apoptosis in human renal tubular
cells through the regulation of cellular oxidative stress, MAPK activation and
restoration of the Bax/Bcl-2 ratio.