Evidence map›Paper›PMID 26775661›Full record

ArticleActa pharmacologica Sinica2016

Emodin ameliorates cisplatin-induced apoptosis of rat renal tubular cells in vitro by activating autophagy.

Hong Liu, Liu-bao Gu, Yue Tu, Hao Hu, Yan-ru Huang, Wei Sun

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

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  11. Emodin ameliorates renal injury and fibrosisFrontiers in pharmacology · 2023
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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

6 authors at 2 institutions in 2 countries.

Hong LiuDepartment of Nephrology, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.
Liu-bao GuCenter for Diabetes Care, Education and Research, Jiangsu Province Institute of Geriatrics, Nanjing 210024, China.
Yue TuDepartment of Graduate School, Nanjing University of Chinese Medicine, Nanjing 210046, China.
Hao HuDepartment of Graduate School, Nanjing University of Chinese Medicine, Nanjing 210046, China.
Yan-ru HuangDepartment of Molecular Signaling, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi 409-3898, Japan.
Wei SunDepartment of Nephrology, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.
Nanjing University of Chinese Medicine · CNUniversity of Yamanashi · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimA previous report shows that emodin extracted from the Chinese herbs rhubarb and giant knotweed rhizome can ameliorate the anticancer drug cisplatin-induced injury of HEK293 cells. In this study, we investigated whether and how emodin could protect renal tubular epithelial cells against cisplatin-induced nephrotoxicity in vitro.

methodsThe viability and apoptosis of normal rat renal tubular epithelial cells (NRK-52E) were detected using formazan assay and flow cytometry analysis, respectively. The expression levels of cleaved caspase-3, autophagy maker LC3 I/II, and AMPK/mTOR signaling pathway-related proteins were measured with Western blot analysis. The changes of morphology and RFP-LC3 fluorescence were observed under microscopy.

resultsCisplatin (10-50 μmol/L) dose-dependently induced cell damage and apoptosis in NRK-52E cells, whereas emodin (10 and 100 μmol/L) significantly ameliorated cisplatin-induced cell damage, apoptosis and caspase-3 cleavage. Emodin dose-dependently increased LC3-II levels and induced RFP-LC3-containing punctate structures in NRK-52E cells. Furthermore, the protective effects of emodin were abolished by bafilomycin A1 (10 nmol/L), and mimicked by rapamycin (100 nmol/L). Moreover, emodin increased the phosphorylation of AMPK and suppressed the phosphorylation of mTOR. The AMPK inhibitor compound C (10 μmol/L) not only abolished emodin-induced autophagy activation, but also emodin-induced anti-apoptotic effects.

conclusionEmodin ameliorates cisplatin-induced apoptosis of rat renal tubular cells in vitro through modulating the AMPK/mTOR signaling pathways and activating autophagy. Emodin may have therapeutic potential for the prevention of cisplatin-induced nephrotoxicity.

Indexed as

AMP-Activated Protein KinasesAnimalsAntineoplastic AgentsApoptosisAutophagyCaspase 3Cell LineCisplatinEmodinHumansKidney TubulesProtective AgentsProtein Kinase InhibitorsRatsSignal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesAntineoplastic AgentsCaspase 3CisplatinEmodinProtective AgentsProtein Kinase InhibitorsTOR Serine-Threonine Kinases

Identifiers

PMID26775661
PMCPMC4753365
OpenAlexW2399586521

What OpenQuestion holds

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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.