Evidence map›Paper›PMID 29568865›Full record

ArticleInternational journal of molecular medicine2018

Trifluoperazine induces apoptosis through the upregulation of Bax/Bcl‑2 and downregulated phosphorylation of AKT in mesangial cells and improves renal function in lupus nephritis mice.

Baodong Wang, Yankun Luo, Xiaoshuang Zhou, Rongshan Li

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. 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
1.3field-weighted citation impact, top 24% 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, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Towards a Unified Approach in Autoimmune Fibrotic Signalling Pathways.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Mesangial cell: A hub in lupus nephritis.Frontiers in immunology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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 1 institution in 1 country.

Baodong WangDepartment of Nephrology, The Affiliated People's Hospital of Shanxi Medical University, Shanxi Provincial People's Hospital, Shanxi Kidney Disease Institute, Taiyuan, Shanxi 030001, P.R. China.
Yankun LuoDepartment of Nephrology, The Affiliated People's Hospital of Shanxi Medical University, Shanxi Provincial People's Hospital, Shanxi Kidney Disease Institute, Taiyuan, Shanxi 030001, P.R. China.
Xiaoshuang ZhouDepartment of Nephrology, The Affiliated People's Hospital of Shanxi Medical University, Shanxi Provincial People's Hospital, Shanxi Kidney Disease Institute, Taiyuan, Shanxi 030001, P.R. China.
Rongshan LiDepartment of Nephrology, The Affiliated People's Hospital of Shanxi Medical University, Shanxi Provincial People's Hospital, Shanxi Kidney Disease Institute, Taiyuan, Shanxi 030001, P.R. China.
Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inhibition of mesangial cell (MC) proliferation has become an important therapy in preventing glomerular proliferation diseases. Trifluoperazine (TFP) has been reported to inhibit the proliferation of several types of cancer cell, however, the effects of TFP in renal proliferation diseases remain to be fully elucidated. The present study examined the effects of TFP on the proliferation of MCs and quantified cell apoptosis progression in vivo and in vitro. The effects of various TFP concentrations and treatment durations on cell proliferation and cell apoptosis in vitro were analyzed using flow cytometry in conjunction with a Cell Counting kit‑8 assay. Cell proliferation in vivo was determined using hematoxylin and eosin staining and immunohistochemistry of Ki67. The expression of the two cell apoptosis‑related proteins, B‑cell lymphoma-2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax), were estimated using western blot analysis and immunohistochemistry in vivo and in vitro. TFP‑induced phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathways were also estimated using western blot analysis. These results suggested that TFP inhibited MC proliferation in a dose‑ and time‑dependent manner. It was found that TFP inhibited the abnormal proliferation of MCs, which was stimulated by 20% fetal bovine serum in vitro and in lupus MRL/lpr mice. TFP promoted cell apoptosis, downregulated the expression of Bcl‑2 and upregulated the expression of Bax in a dose‑dependent manner at mRNA and protein levels. In addition, TFP inhibited phosphorylated AKT, potentially leading to the suppressed activation of PI3K/AKT signaling pathways. TFP treatment significantly decreased the levels of blood urea nitrogen and serum creatinine, but had no significant effects on the body weight and liver function of the lupus mice. These results validated and reinforced the potential of TFP in the treatment of mesangial proliferative diseases.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCell ProliferationFemaleLupus NephritisMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTrifluoperazinebcl-2-Associated X ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTrifluoperazine

Identifiers

PMID29568865
PMCPMC5881739
OpenAlexW2791212454

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.