Evidence map›Paper›PMID 26230340›Full record

ArticlePloS one2015

Panaxadiol Saponin and Dexamethasone Improve Renal Function in Lipopolysaccharide-Induced Mouse Model of Acute Kidney Injury.

Yan Chen, Yanwei Du, Yang Li, Xiaoqin Wang, Pin Gao, Guang Yang, Yuan Fang, Yan Meng, Xuejian Zhao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 43 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

9 authors at 2 institutions in 1 country.

Yan ChenDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China; Department of Nephropathy, The First Hospital of Jilin University, Changchun, China.
Yanwei DuDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Yang LiDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Xiaoqin WangDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Pin GaoDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Guang YangDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Yuan FangDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Yan MengDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Xuejian ZhaoDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, China.
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) is a serious complication of systemic inflammatory response syndrome (SIRS), which has a high mortality rate. Previous studies showed that panaxadiol saponin (PDS) and Dexamethasone have similar anti-inflammatory properties and protect cardiopulmonary function in lipopolysaccharide (LPS)-induced septic shock rats. In the present study, we investigated whether PDS or Dexamethasone has a similar role in improving kidney function in LPS-induced AKI mice. METHODS AND

resultsMice subjected to LPS (10 mg/kg) treatment exhibited AKI demonstrated by markedly increased blood urea nitrogen and creatinine levels compared with controls (P<0.01). However, PDS and Dexamethasone induce similar reverse effects on renal function, such as reduced serum creatinine and blood urea nitrogen levels compared with the LPS group (P<0.05). PDS decreased the production and release of tumor necrosis factor (TNF)-α and interleukin (IL)-6 by inhibiting the NF-κB signaling pathway, down-regulating inducible nitric oxide synthase protein expression levels and inhibiting oxidative stress. In most anti-AKI mechanisms, PDS and dexamethasone were similar, but PDS are better at inhibition of TNF production, promote SOD activity and inhibition of IKB phosphorylation. In addition, nuclear glucocorticoid receptor expression was markedly enhanced in PDS and Dexamethasone treatment groups. Further research is required to determine whether PDS can combine with the glucocorticoid receptor to enter the nucleus.

conclusionThis study demonstrated that PDS and dexamethasone have similar reverse amelioration for renal functions, and have potential application prospects in the treatment of sepsis-induced AKI.

Indexed as

Acute Kidney InjuryAnimalsDexamethasoneDisease Models, AnimalGinsenosidesKidneyLipopolysaccharidesMalondialdehydeMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIReceptors, GlucocorticoidSuperoxide DismutaseDexamethasoneGinsenosidesLipopolysaccharidesMalondialdehydeNitric OxideNitric Oxide Synthase Type IIpanaxadiolReceptors, GlucocorticoidSuperoxide Dismutase

Identifiers

PMID26230340
PMCPMC4521715
OpenAlexW1762558009

What OpenQuestion holds

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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.