Evidence map›Paper›PMID 29669072›Full record

ArticleJournal of animal science2018

Vitamin A pretreatment protects NO-induced bovine mammary epithelial cells from oxidative stress by modulating Nrf2 and NF-κB signaling pathways.

H Y Shi, S M Yan, Y M Guo, B Q Zhang, X Y Guo, B L Shi

Abstract read
In one paragraph

Article in Journal of animal science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Role of vitamins in the development and treatment of osteoporosis (Review).International journal of molecular medicine · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Relationship between Vitamin D and Immunity in Older People with COVID-19.International journal of environmental research and public health · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Anti-Inflammatory CeOMolecules (Basel, Switzerland) · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

H Y ShiCollege of Animal Science, Inner Mongolia Agricultural University, Hohhot, P.R. China.
S M YanCollege of Animal Science, Inner Mongolia Agricultural University, Hohhot, P.R. China.
Y M GuoCollege of Animal Science, Inner Mongolia Agricultural University, Hohhot, P.R. China.
B Q ZhangCollege of Animal Science, Inner Mongolia Agricultural University, Hohhot, P.R. China.
X Y GuoCollege of Animal Science, Inner Mongolia Agricultural University, Hohhot, P.R. China.
B L ShiCollege of Animal Science, Inner Mongolia Agricultural University, Hohhot, P.R. China.
Inner Mongolia Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is known that physiological overproduction of nitric oxide (NO) contributes to oxidative stress and inflammation. Our published studies indicated that vitamin A (VA) reduces NO-induced oxidative stress in bovine mammary epithelial cells (BMECs) by increasing antioxidant enzyme activities. However, the precise mechanism is unclear. The present study was conducted to examine the protective effects of VA on NO-induced damage to BMECs in vitro using diethylenetriamine nitric oxide (DETA-NO) as the NO donor and to explore the intracellular signaling mechanisms of VA that involve nuclear factor erythroid 2-related factor (Nrf2) and nuclear factor kappa-B (NF-κB). Subconfluent BMECs were divided into 10 treatment groups with 6 replicates per treatment and were cultured with dimethyl sulfoxide (DMSO, vehicle negative control) or 0, 0.05, 0.1, 0.2, 0.5, 1, 2, 3, or 4 μg/mL of VA for 24 h and then incubated in the absence or presence of DETA-NO (1,000 μmol/liter) and VA for an additional 6 h. The results showed that exposure to DETA alone decreased cell proliferation compared with the negative control. Pretreatment with VA promoted the proliferation of BMECs, increased the activities of antioxidative enzymes including selenoprotein glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) and their gene and protein expression but decreased NO and interleukin 1 (IL-1) contents in a quadratic manner (P < 0.05). In addition, the expression of mRNA and protein of factors that are related to NF-κB or Nrf2 signaling pathways in BMECs were regulated by VA in a quadratic dose-dependent manner; VA at a concentration of 1 μg/mL exhibited the strongest effect. Together, these results suggest that VA promotes antioxidant functions of BMECs by regulating the synthesis of selenoproteins including GPx and TrxR and by reducing concentrations of IL-1 and NO in vitro by modulating Nrf2 and NF-κB signaling pathways.

Indexed as

AnimalsAntioxidantsCattleCell ProliferationCells, CulturedEpithelial CellsFemaleInflammationMammary Glands, AnimalNF-E2-Related Factor 2NF-kappa BNitric OxideOxidative StressSignal TransductionVitamin AAntioxidantsNF-E2-Related Factor 2NF-kappa BNitric OxideVitamin A

Identifiers

PMID29669072
PMCPMC6140872
OpenAlexW2796837402

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.