Evidence map›Paper›PMID 26576227›Full record

ArticleOxidative medicine and cellular longevity2015

Lico A Enhances Nrf2-Mediated Defense Mechanisms against t-BHP-Induced Oxidative Stress and Cell Death via Akt and ERK Activation in RAW 264.7 Cells.

Hongming Lv, Hua Ren, Lidong Wang, Wei Chen, Xinxin Ci

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. [Licochalcone A induces cell cycle arrest in human lung squamous carcinoma cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  6. Article
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  11. Anti-Inflammatory and Antioxidant Effects ofMediators of inflammation · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Toxicology research · 2018
    Article
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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

5 authors at 1 institution in 1 country.

Hongming LvInstitute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China ; Key Laboratory of Zoonosis Research, Ministry of Education, College of Animal Science and Veterinary Medicine, Jilin University, 5333 Xi'an Road, Changchun 130062, China.
Hua RenInstitute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China.
Lidong WangInstitute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China.
Wei ChenKey Laboratory of Zoonosis Research, Ministry of Education, College of Animal Science and Veterinary Medicine, Jilin University, 5333 Xi'an Road, Changchun 130062, China.
Xinxin CiInstitute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Licochalcone A (Lico A) exhibits various biological properties, including anti-inflammatory and antioxidant activities. In this study, we investigated the antioxidative potential and mechanisms of Lico A against tert-butyl hydroperoxide- (t-BHP-) induced oxidative damage in RAW 264.7 cells. Our results indicated that Lico A significantly inhibited t-BHP-induced cytotoxicity, apoptosis, and reactive oxygen species (ROS) generation and reduced glutathione (GSH) depletion but increased the glutamate-cysteine ligase modifier (GCLM) subunit and the glutamate-cysteine ligase catalytic (GCLC) subunit genes expression. Additionally, Lico A dramatically upregulated the antioxidant enzyme heme oxygenase 1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2), which were associated with inducing Nrf2 nuclear translocation, decreasing Keap1 protein expression and increasing antioxidant response element (ARE) promoter activity. Lico A also obviously induced the activation of serine/threonine kinase (Akt) and extracellular signal-regulated kinase (ERK), but PI3K/Akt and ERK inhibitors treatment displayed clearly decreased levels of LicoA-induced Nrf2 nuclear translocation and HO-1 expression, respectively. Furthermore, Lico A treatment markedly attenuated t-BHP-induced oxidative damage, which was reduced by treatment with PI3K/Akt, ERK, and HO-1 inhibitors. Therefore, Lico A might have a protective role against t-BHP-induced cytotoxicity by modulating HO-1 and by scavenging ROS via the activation of the PI3K/Akt and ERK/Nrf2 signaling pathways.

Indexed as

AnimalsAntioxidant Response ElementsApoptosisCell SurvivalChalconesExtracellular Signal-Regulated MAP KinasesGlutamate-Cysteine LigaseHeme Oxygenase-1MiceNF-E2-Related Factor 2Oxidative StressPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPromoter Regions, GeneticProto-Oncogene Proteins c-aktRAW 264.7 CellsChalconesExtracellular Signal-Regulated MAP KinasesGCLM protein, mouseGlutamate-Cysteine LigaseHeme Oxygenase-1licochalcone ANF-E2-Related Factor 2Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReactive Oxygen Speciestert-Butylhydroperoxide

Identifiers

PMID26576227
PMCPMC4630662
OpenAlexW1776086334

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.