Evidence map›Paper›PMID 29071538›Full record

ArticleMolecular and cellular biochemistry2018

Total flavone of Desmodium styracifolium relieved apoptosis and autophagy of COM-induced HK-2 cells by regulating KIM-1 via p38/MAPK pathway.

Haijie Xie, Jie Li, Hongwei Gao, Jun Wang, Chuanbo Li, Yong Xu, Chunyu Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  10. Heliyon · 2024
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  12. Carboxymethylation ofOxidative medicine and cellular longevity · 2022
    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

7 authors at 2 institutions in 1 country.

Haijie XieUrolithiasis Treatment Center of Tianjin, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China.
Jie LiUrolithiasis Treatment Center of Tianjin, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China.
Hongwei GaoUrolithiasis Treatment Center of Tianjin, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China.
Jun WangUrolithiasis Treatment Center of Tianjin, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China.
Chuanbo LiUrolithiasis Treatment Center of Tianjin, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China.
Yong XuUrolithiasis Treatment Center of Tianjin, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China. yong_xu234@163.com.
Chunyu LiuUrolithiasis Treatment Center of Tianjin, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China. ChunYu_Liu234@163.com.
Second Hospital of Tianjin Medical University · CNTianjin Medical University · CN

Funding

the Traditional Chinese medicine and Western Medicine Research of Tianjin health and Family Planning Commission 2015134
6 · The paper itself

Abstract

The purpose of the study was to investigate the mechanism of total flavone of Desmodium styracifolium (TFDS) in regulating the formation of urinary calculi. Protein levels of KIM-1, LC3-II, p-p38 were measured by Western blot. The effect of different COM concentrations, different TFDS concentrations, SB203580 (specific inhibitor of p38/MAPK), and overexpression of KIM-1 on cell viability were detected by WST-1 assay. The apoptotic cells and FITC positive cells were detected by flow cytometry. HK-2 cell viability decreased with the increase of COM concentration, and the protein levels of KIM-1, LC3-II, and p-p38 increased with the time. Blocking the p38/MAPK pathway or co-cultured with TFDS inhibited the effects of COM on apoptosis and autophagy of HK-2 cells. In addition, blocking the p38/MAPK pathway inhibited the expression of KIM-1. In COM-induced cells, after treated with SB203580, overexpression of KIM-1 could reverse the protection effect of SB203580 on COM-induced cell damage and the inhibition of SB203580 on COM-induced excessive autophagy, suggesting p38/MAPK regulated KIM-1 to regulate COM-induced cell apoptosis and autophagy. Finally, we proved that TFDS inhibited p38/MAPK pathway. And the protection effect of COM-induced cell injury increased with the increase of TFDS concentration, and the adhesion between COM and cells decreased with the increase of TFDS concentration. With the increase of the concentration of TFDS, p38/MAPK pathway was gradually inhibited, and KIM-1 and autophagy related proteins were decreased. TFDS inhibited HK-2 cell apoptosis and autophagy by regulating KIM-1 via p38/MAPK pathway.

Indexed as

ApoptosisAutophagyCell LineFabaceaeFlavonesHepatitis A Virus Cellular Receptor 1HumansMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesflavoneFlavonesHAVCR1 protein, humanHepatitis A Virus Cellular Receptor 1p38 Mitogen-Activated Protein KinasesKIM-1LC3-IIp38/MAPKTotal flavone of Desmodium styracifolium

Identifiers

PMID29071538
OpenAlexW2765421154

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.