Evidence map›Paper›PMID 33394221›Full record

ArticleNeurochemical research2021

Platycodin D Inhibits β-Amyloid-Induced Inflammation and Oxidative Stress in BV-2 Cells Via Suppressing TLR4/NF-κB Signaling Pathway and Activating Nrf2/HO-1 Signaling Pathway.

Jing Zhang, Na Song, Yuzhi Liu, Junwei Guo

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Frontiers in nutrition · 2024
    Article
  10. Review
  11. Review
  12. Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Article
  15. 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

4 authors at 3 institutions in 1 country.

Jing ZhangNursing Department, Aviation General Hospital, Beijing, 100012, China.
Na SongSecond Ward, Binzhou Youfu Hospital of Shandong Province, Binzhou, 256600, Shandong, China.
Yuzhi LiuFemale Ward, Binzhou Youfu Hospital of Shandong Province, Binzhou, 256600, Shandong, China.
Junwei GuoPsychological Outpatient Department, Chongqing Traditional Chinese Medicine Hospital, Chongqing, 404000, China. junweiguo01@163.com.
Aviation General Hospital · CNFirst People's Hospital of Chongqing · CNWuhan Youfu Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a common neurodegenerative disease associated with deposition of β-amyloid peptide (Aβ). Platycodin D (PLD), a triterpenesaponin, may possess neuro-protective effect. In the current study, we aimed to explore the effects of PLD on Aβ-induced inflammation and oxidative stress in microglial BV-2 cells. Our study showed that PLD treatment improved cell viability in Aβ-induced BV-2 cells. PLD attenuated Aβ-induced inflammation with deceased production of TNF-α, IL-1β and IL-6 in Aβ-induced BV-2 cells. PLD also mitigated the oxidative stress in Aβ-induced BV-2 cells, as evidenced by deceased production of ROS and MDA, and increased SOD activity. Furthermore, the increased expression levels of TLR4 and p-p65 and decreased IκBα expression in the Aβ-stimulated BV-2 cells were attenuated by PLD treatment. Overexpression of TLR4 reversed the anti-inflammatory effect of PLD in Aβ-stimulated BV-2 cells. In addition, PLD treatment enhanced the Aβ-stimulated increase in the expression levels of Nrf2, HO-1, and NQO1 in BV-2 cells. Knockdown of Nrf2 abrogated the anti-oxidative effect of PLD in Aβ-stimulated BV-2 cells. In conclusion, these findings indicated that PLD protected BV-2 cells from Aβ-induced oxidative stress and inflammation via regulating the TLR4/NF-κB and Nrf2/HO-1 signaling pathways. Thus, PLD may be a potential candidate for the treatment of AD.

Indexed as

Amyloid beta-PeptidesAnimalsCell LineCell SurvivalGene Knockdown TechniquesHeme Oxygenase-1InflammationMembrane ProteinsMiceNF-E2-Related Factor 2NF-kappa B p50 SubunitOxidative StressPeptide FragmentsSaponinsSignal TransductionToll-Like Receptor 4Amyloid beta-Peptidesamyloid beta-protein (1-42)Heme Oxygenase-1Hmox1 protein, mouseMembrane ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2NF-kappa B p50 SubunitNfkb1 protein, mousePeptide Fragmentsplatycodin DSaponinsTlr4 protein, mouseToll-Like Receptor 4TriterpenesAlzheimer’s disease (AD)InflammationNrf2/HO-1 signaling pathwayOxidative stressPlatycodin D (PLD)TLR4/NF-κb signaling pathway

Identifiers

PMID33394221
OpenAlexW3119637362

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.