Evidence map›Paper›PMID 26576221›Full record

ArticleOxidative medicine and cellular longevity2015

Nephroprotective Effects of Polydatin against Ischemia/Reperfusion Injury: A Role for the PI3K/Akt Signal Pathway.

Hong-Bao Liu, Qiu-Hong Meng, Chen Huang, Jian-Bo Wang, Xiao-Wei Liu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.7field-weighted citation impact, top 5% 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, 73 citations in OpenAlex.

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  19. Effect of Lipopolysaccharide fromArchives of Razi Institute · 2021
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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

5 authors at 2 institutions in 1 country.

Hong-Bao LiuDepartment of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China ; State Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Fourth Military Medical University, Xi'an 710032, China.
Qiu-Hong MengInstitute of Materia Medica, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Chen HuangDepartment of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Jian-Bo WangInstitute of Materia Medica, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
Xiao-Wei LiuDepartment of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and inflammation are involved in the pathogenesis in renal ischemia/reperfusion (I/R) injury. It has been demonstrated that polydatin processed the antioxidative, anti-inflammatory, and nephroprotective properties. However, whether it has beneficial effects and the possible mechanisms on renal I/R injury remain unclear. In our present study I/R models were simulated both in vitro and in vivo. Compared with vehicle control, the administration of polydatin significantly improved the renal function, accelerated the mitogenic response and reduced cell apoptosis in renal I/R injury models, strongly suppressed the I/R-induced upregulation of the expression of tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase, prostaglandin E-2, and nitric oxide levels, and dramatically decreased contents of malondialdehyde, but it increased the activity of superoxide dismutase, glutathione transferase, glutathione peroxidase and catalase, and the level of glutathione. Further investigation showed that polydatin upregulated the phosphorylation of Akt in kidneys of I/R injury dose-dependently. However, all beneficial effects of polydatin mentioned above were counteracted when we inhibited PI3K/Akt pathway with its specific inhibitor, wortmannin. Taken together, the present findings provide the first evidence demonstrating that PD exhibited prominent nephroprotective effects against renal I/R injury by antioxidative stress and inflammation through PI3-K/Akt-dependent molecular mechanisms.

Indexed as

AnimalsAntioxidantsCyclooxygenase 2Disease Models, AnimalGlucosidesInterleukin-1betaKidneyMaleMiceMice, Inbred BALB CNitric Oxide Synthase Type IIOxidative StressOxidoreductasesPhosphatidylinositol 3-KinasesProtective AgentsProto-Oncogene Proteins c-aktAntioxidantsCyclooxygenase 2GlucosidesInterleukin-1betaNitric Oxide Synthase Type IIOxidoreductasesPhosphatidylinositol 3-KinasespolydatinProtective AgentsProto-Oncogene Proteins c-aktStilbenesTumor Necrosis Factor-alpha

Identifiers

PMID26576221
PMCPMC4630419
OpenAlexW2139832080

What OpenQuestion holds

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LicenceCC BY
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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.