Evidence map›Paper›PMID 27229751›Full record

ArticleScientific reports2016

Corosolic acid inhibits the proliferation of glomerular mesangial cells and protects against diabetic renal damage.

Xiao-Qiang Li, Wen Tian, Xiao-Xiao Liu, Kai Zhang, Jun-Cheng Huo, Wen-Juan Liu, Ping Li, Xiong Xiao, Ming-Gao Zhao, Wei Cao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 44 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Xiao-Qiang LiDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Wen TianDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Xiao-Xiao LiuDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Kai ZhangDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Jun-Cheng HuoCadet Brigade, Fourth Military Medical University, Xi'an 710032, China.
Wen-Juan LiuDepartment of Natural Medicine &Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Ping LiDepartment of Natural Medicine &Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Xiong XiaoDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Ming-Gao ZhaoDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Wei CaoDepartment of Natural Medicine &Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is one of the major complications of diabetes mellitus (DM). This study aimed to explore the effects of corosolic acid (CA) on the renal damage of DM and the mechanisms behind these effects. The renoprotective effect of CA was investigated in type 1 diabetic rats and db/db mice. The kidneys and glomerular mesangial cells (GMCs) were used to study the proliferation of GMCs by immunostaining and MTT assay. Further immunoblotting, siRNA, qPCR analysis, and detecting of NADPH oxidase activity and reactive oxygen species (ROS) generation were performed to explore relevant molecular mechanisms. In CA-treated diabetic animals, diabetes-induced albuminuria, increased serum creatinine and blood urea nitrogen were significantly attenuated, and glomerular hypertrophy, mesangial expansion and fibrosis were ameliorated. Furthermore, CA significantly inhibited proliferation of GMCs and phosphorylation of ERK1/2 and p38 MAPK in both diabetic animals and high glucose (HG)-induced GMCs. CA also normalized Δψm and inhibited HG-induced NADPH oxidase activity, ROS generation and NOX4, NOX2, p22(phox) and p47(phox) expression. More importantly, CA inhibited GMC proliferation mediated by NADPH/ERK1/2 and p38 MAPK signaling pathways. These findings suggest that CA exert the protective effect on DN by anti-proliferation resulted from inhibition of p38 MAPK- and NADPH-mediated inactivation of ERK1/2.

Indexed as

AnimalsBlood GlucoseCell ProliferationDiabetes Mellitus, ExperimentalDiabetic NephropathiesMaleMAP Kinase Signaling SystemMesangial CellsMice, Inbred C57BLNADPH OxidasesReactive Oxygen SpeciesTriterpenesBlood Glucosecorosolic acidNADPH OxidasesReactive Oxygen SpeciesTriterpenes

Identifiers

PMID27229751
PMCPMC4882506
OpenAlexW2400650732

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.