Evidence map›Paper›PMID 32285909›Full record

ArticleBioscience reports2020

Anti-apoptosis mechanism of triptolide based on network pharmacology in focal segmental glomerulosclerosis rats.

Yayu Li, Xue Jiang, Litao Song, Mengdie Yang, Jing Pan

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Therapeutic potential ofFrontiers in pharmacology · 2023
    Article
  3. Review
  4. Article
  5. Review
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Yayu LiDepartment of Nephrology, Guangxing Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou Hospital of Traditional Chinese Medicine, No. 453, Tiyuchang Road, Hangzhou City, Zhejiang Province 310007, P. R. China.
Xue JiangDepartment of Nephrology, Guangxing Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou Hospital of Traditional Chinese Medicine, No. 453, Tiyuchang Road, Hangzhou City, Zhejiang Province 310007, P. R. China.
Litao SongDepartment of Nephrology, Hangzhou Dingqiao Hospital, Dingqiao Branch of Hangzhou Hospital of Traditional Chinese medicine, No. 453, Tiyuchang Road, Hangzhou City, Zhejiang Province 310007, P. R. China.
Mengdie YangDepartment of Nephrology, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, No. 548, Binwen Road, Hangzhou City, Zhejiang Province 310000, P. R. China.
Jing PanDepartment of Nephrology, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, No. 548, Binwen Road, Hangzhou City, Zhejiang Province 310000, P. R. China.
Zhejiang Chinese Medical University · CNHangzhou Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triptolide (TPL), the active component of Tripterygium wilfordii, exhibits anti-cancer and antioxidant functions. We aimed to explore the anti-apoptosis mechanism of TPL based on network pharmacology and in vivo and in vitro research validation using a rat model of focal segmental glomerulosclerosis (FSGS). The chemical structures and pharmacological activities of the compounds reported in T. wilfordii were determined and used to perform the network pharmacology analysis. The Traditional Chinese Medicine Systems Pharmacology Database (TCMSP) was then used to identify the network targets for 16 compounds from Tripterygium wilfordii. Our results showed that 47 overlapping genes obtained from the GeneCards and OMIM databases were involved in the occurrence and development of FSGS and used to construct the protein-protein interaction (PPI) network using the STRING database. Hub genes were identified via the MCODE plug-in of the Cytoscape software. IL4 was the target gene of TPL in FSGS and was mainly enriched in the cell apoptosis term and p53 signaling pathway, according to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. TPL inhibited FSGS-induced cell apoptosis in rats and regulated IL4, nephrin, podocin, and p53 protein levels via using CCK8, TUNEL, and Western blot assays. The effects of IL4 overexpression, including inhibition of cell viability and promotion of apoptosis, were reversed by TPL. TPL treatment increased the expression of nephrin and podocin and decreased p53 expression in rat podocytes. In conclusion, TPL inhibited podocyte apoptosis by targeting IL4 to alleviate kidney injury in FSGS rats.

Indexed as

apoptosisFSGSIL4network pharmacologytriptolide

Identifiers

PMID32285909
PMCPMC7189607
OpenAlexW3016231303

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.