Evidence map›Paper›PMID 26956469›Full record

ArticleInflammation2016

CSTMP Exerts Anti-Inflammatory Effects on LPS-Induced Human Renal Proximal Tubular Epithelial Cells by Inhibiting TLR4-Mediated NF-κB Pathways.

Yan Ding, Wang Liao, Xiaojie He, Wei Xiang, Qianjin Lu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Paeoniflorin Inhibits LPS-Induced Activation of Splenic CD4Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Baicalein alleviates tubular-interstitial nephritis in vivo and in vitro by down-regulating NF-κB and MAPK pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
  10. Article
  11. The peptide lycosin-I attenuates TNF-α-induced inflammation in human umbilical vein endothelial cells via IκB/NF-κB signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    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

5 authors at 3 institutions in 1 country.

Yan DingDepartment of Dermatology, Hainan General Hospital, Haikou, 570102, China.
Wang LiaoDepartment of Cardiology, Hainan General Hospital, Haikou, 570102, China.
Xiaojie HeDepartment of Nephropathy, Children's Medical Center, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Wei XiangDepartment of Pediatrics, Maternal and Child Health care Hospital of Hainan Province, 15 Long Kun-Nan Road, Haikou, 570206, China. xiangweihn2@163.com.
Qianjin LuDepartment of Dermatology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Hainan Maternal and Child Health Hospital · CNSecond Xiangya Hospital of Central South University · CNHainan General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

(E)-2-(2-chlorostyryl)-3,5,6-trimethylpyrazine (CSTMP), a novel stilbene derivative, have been shown to have cytoprotective effects against H2O2-induced oxidative stress in human endothelial cells. However, little is known about its anti-inflammatory effects in lupus nephritis (LN). In the present study, we investigated the anti-inflammatory effects of CSTMP on lipopolysaccharide (LPS)-induced human renal proximal tubular epithelial cells (hRPTECs) and elucidated its molecular mechanisms. CSTMP significantly attenuated the cytotoxicity and suppressed the release of proinflammatory mediators, including iNOS, COX-2, TNF-α, IL-6, IL-8, CCL-2, ICAM-1, IL-1β, and MCP-1 in LPS-induced hRPTECs. In addition, CSTMP decreased the expression of TLR4 and its adapter molecules (MyD88, phosphorylation of TAK1, TRAF6, and IRAK1) and abolished its interactions with these adapter molecules in LPS-induced hRPTECs, resulting in an inhibition of the TLR4/MyD88/TAK1/ TRAF6/IRAK1 complex. Moreover, CSTMP also attenuated phosphorylation of IκB and IKK-α/β, and P50-NF-κB and P65-NF-κB translocation to nucleus in LPS-induced hRPTECs. These findings provided new insights to understand the mode of action of CSTMP in treatment of inflammatory diseases, such as LN.

Indexed as

Active Transport, Cell NucleusAnti-Inflammatory AgentsCells, CulturedEpithelial CellsHumansHydrogen PeroxideI-kappa B KinaseInflammation MediatorsInterleukin-1 Receptor-Associated KinasesKidney Tubules, ProximalLipopolysaccharidesLupus NephritisMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMyeloid Differentiation Factor 88NF-kappa B2-(2-chlorostyryl)-3,5,6-trimethylpyrazineAnti-Inflammatory AgentsHydrogen PeroxideI-kappa B KinaseInflammation MediatorsInterleukin-1 Receptor-Associated KinasesIRAK1 protein, humanLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitPyrazinesRELA protein, humanStilbenesTLR4 protein, humanTNF Receptor-Associated Factor 6Toll-Like Receptor 4Transcription Factor RelACSTMPhuman renal proximal tubular epithelial cellsinflammatory responseNF-κBTLR4

Identifiers

PMID26956469
OpenAlexW2294593089

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.