摘要：Introduction
Correction to:
Scientific Reports 10.1038/s41598-017-11512-6, published online 13 September 2017
The original version of this Article contained an error in Figure 3a where the oxidative lesion applied was incorrect,
“300 µM t-BHP”
now reads:
“300 µM H
2O
2”
Moreover, the original version of this Article also contained an error in Figure 3b where the glutamate excitotoxicity was incorrect,
“300 µM H
2O
2”
now reads:
“100 µM glutamate”
The figure legend was correct at the time of publication. The original Figure
3 and accompanying legend appear below.
The original Article has been corrected.
Figure 3
Cytoprotective potential of Cat-sulf and Pyr-sulf. (
a) HBMEC line submitted to oxidative stress (300 µM H
2O
2); (
b) primary mouse cerebellar granule cells exposed to glutamate excitotoxicity (100 µM glutamate); (
c) 3D aggregates containing neurons and astrocytes exposed to oxidative injury (300 µM
t-BHP). Cells were pre-incubated with 5 µM of each bioavailable polyphenol metabolite for 24 h and then injured with the respective lesion. Cell viability was assessed and is presented as percentage relatively to control. Statistical differences are denoted as ***p < 0.001, **p < 0.01 and *p < 0.05 relatively to control and as
###p < 0.001,
##p < 0.01 and
# p < 0.05 relatively to each lesion (H
2O
2, glutamate or
t-BHP). (
d–f) Alterations in protein markers of the neuronal (β-III tubulin) and astrocytic (GFAP) population of 3D aggregates towards the
t-BHP lesion without and with pre-incubation with idebenone (Ide), a control drug, and with Pyr-sulf. (
d) Representative western blot and (
e) β-III tubulin and (
f) GFAP fold changes in protein levels normalized to GAPDH. Statistical differences are denoted as ***p < 0.001, **p < 0.01 and *p < 0.05 relatively to control and as
###p < 0.001 relatively to
t-BHP. Western blots were analyzed under the same experimental conditions. Data are presented as the means ± SD, n = 3.
