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. 2019 Jan 14;22:101101. doi: 10.1016/j.redox.2019.101101

Corrigendum to “Polydatin prevents fructose-induced liver inflammation and lipid deposition through increasing miR-200a to regulate Keap1/Nrf2 pathway” [Redox Biol. 18 (2018) 124–137]

Xiao-Juan Zhao 1, Han-Wen Yu 1, Yan-Zi Yang 1, Wen-Yuan Wu 1, Tian-Yu Chen 1, Ke-Ke Jia 1, Lin-Lin Kang 1, Rui-Qing Jiao 1, Ling-Dong Kong 1
PMCID: PMC6435944  PMID: 30655077

The authors regret In the article referenced above, a picture error was inadvertently introduced during the course of revision. There was a copy and paste error in Fig. 1C where the right-most column of representative microphotographs of oil-red O-stained paraffin-embedded sections of rat liver tissues from pioglitazone treatment group (4 mg/kg Pioglitazone with fructose intake) was wrongly presented as a copy of the left one (15 mg/kg Polydatin with fructose intake). In the corrigendum figure, we have provided correct microphotographs of rat liver oil-red O staining from 4 mg/kg Pioglitazone with fructose intake. All the authors have been made aware of this error and have agreed to its correction. The authors regret any inconvenience to readers arising from the error.

Corrected Fig. 1.

Corrected Fig. 1

Polydatin alleviates liver inflammation and lipid deposition in fructose-fed rats. Rats were fed 10% fructose drinking water (wt/vl) for 13 weeks and treated with polydtain (7.5, 15, 30 mg/kg) and pioglitazone (4 mg/kg) during the last 7 weeks. (A) qRT-PCR analysis of TXNIP mRNA levels, and (B) Western blot analysis of TXNIP protein levels in rat livers (n = 4 at least). Relative mRNA levels of TXNIP were normalized to β-actin. Relative protein levels of TXNIP were normalized to GAPDH. (C) Representative microphotograph of H&E-stained and oil-red O-stained paraffin-embedded sections of liver tissues were shown (200 and 400 × magnification; bars, 100 µm), respectively. (D) Western blot analysis of NLRP3, ASC, Caspase-1, IL-1β, PPAR-α, CPT-1, SREBP-1 and SCD-1 protein levels in rat livers (n = 4 at least). Relative protein levels of Caspase-1 were normalized to pro-Caspase-1, of IL-1β were normalized to pro-IL-1β, of TXNIP, NLRP3, ASC, PPAR-α, CPT-1, SREBP-1 and SCD-1 were normalized to GAPDH or β-actin, respectively. All data are expressed as mean ± S.E.M. P value was calculated by one-way ANOVA and further post hoc Dunnett testing. #P < 0.05, ##P < 0.01, ###P < 0.001 compared with control-vehicle; *P < 0.05, **P < 0.01, ***P < 0.001 compared with fructose-vehicle. TXNIP, thioredoxin-interacting protein; NLRP3, The NOD-like receptor (NLR) family, pyrin domain containing 3; ASC, apoptosis-associated speck-like protein; IL-1β, interleukin-1β; PPAR-α, peroxisome proliferator activated receptor-α; CPT-1, carnitine palmitoyl transferase-1; SREBP-1, sterol regulatory element binging protein 1; SCD-1, stearoyl-CoA desaturase-1.

The authors would like to apologise for any inconvenience caused.


Articles from Redox Biology are provided here courtesy of Elsevier

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