Evidence map›Paper›PMID 27057271›Full record

ArticleOxidative medicine and cellular longevity2016

Polydatin Protecting Kidneys against Hemorrhagic Shock-Induced Mitochondrial Dysfunction via SIRT1 Activation and p53 Deacetylation.

Zhenhua Zeng, Zhongqing Chen, Siqi Xu, Qin Zhang, Xingmin Wang, Youguang Gao, Ke-seng Zhao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 66 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

7 authors at 3 institutions in 1 country.

Zhenhua ZengDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Guangdong Key Lab of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University, Guangzhou 510515, China.
Zhongqing ChenDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Siqi XuGuangdong Key Lab of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University, Guangzhou 510515, China.
Qin ZhangDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Xingmin WangGuangdong Key Lab of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University, Guangzhou 510515, China.
Youguang GaoDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Anesthesiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005, China.
Ke-seng ZhaoGuangdong Key Lab of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University, Guangzhou 510515, China.
Southern Medical University · CNNanfang Hospital · CNFirst Affiliated Hospital of Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo ascertain if mitochondrial dysfunction (MD) of kidney cells is present in severe hemorrhagic shock and to investigate whether polydatin (PD) can attenuate MD and its protective mechanisms. RESEARCH DESIGN AND

methodsRenal tubular epithelial cells (RTECs) from rat kidneys experiencing HS and a cell line (HK-2) under hypoxia/reoxygenation (H/R) treatment were used. Morphology and function of mitochondria in isolated RTECs or cultured HK-2 cells were evaluated, accompanied by mitochondrial apoptosis pathway-related proteins.

resultSevere MD was found in rat kidneys, especially in RTECs, as evidenced by swollen mitochondria and poorly defined cristae, decreased mitochondrial membrane potential (ΔΨm), and reduced ATP content. PD treatment attenuated MD partially and inhibited expression of proapoptotic proteins. PD treatment increased SIRT1 activity and decreased acetylated-p53 levels. Beneficial effect of PD was abolished partially when the SIRT1 inhibitor Ex527 was added. Similar phenomena were shown in the H/R cell model; when pifithrin-α (p53 inhibitor) was added to the PD/Ex527 group, considerable therapeutic effects were regained compared with the PD group apart from increased SIRT1 activity.

conclusionsMD is present in severe HS, and PD can attenuate MD of RTECs via the SIRT1-p53 pathway. PD might be a promising therapeutic drug for acute renal injury.

Indexed as

AnimalsBlotting, WesternCarbazolesCell HypoxiaCells, CulturedFemaleGlucosidesImmunohistochemistryKidneyMaleMembrane Potential, MitochondrialMitochondriaOxygenProtective AgentsRatsRats, Sprague-Dawley6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamideCarbazolesGlucosidesOxygenpolydatinProtective AgentsSirtuin 1StilbenesTumor Suppressor Protein p53

Identifiers

PMID27057271
PMCPMC4783550
OpenAlexW2276884332

What OpenQuestion holds

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LicenceCC BY
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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.