Evidence map›Paper›PMID 31641228›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2020

Polydatin protects against lipopolysaccharide-induced endothelial barrier disruption via SIRT3 activation.

Jie Wu, Zhiya Deng, Maomao Sun, Weijin Zhang, Yang Yang, Zhenhua Zeng, Jianhua Wu, Qin Zhang, Yanan Liu, Zhenfeng Chen and 4 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2020. 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
2.9field-weighted citation impact, top 9% 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, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Brazilin alleviates acute lung injury via inhibition of ferroptosis through the SIRT3/GPX4 pathway.Apoptosis : an international journal on programmed cell death · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Surgical infections · 2023
    Article
  15. Article
  16. Annals of translational medicine · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. Review
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

14 authors at 2 institutions in 1 country.

Jie Wu *Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Zhiya Deng *Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Maomao SunDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Weijin ZhangDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yang YangDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Zhenhua ZengDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Jianhua WuThe First School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, China.
Qin ZhangDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yanan LiuDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Zhenfeng ChenGuangdong Provincial Key Lab of Shock and Microcirculation, Department of Pathophysiology, Southern Medical University, Guangzhou, 510515, China.
Xiaohua GuoGuangdong Provincial Key Lab of Shock and Microcirculation, Department of Pathophysiology, Southern Medical University, Guangzhou, 510515, China.ORCID http://orcid.org/0000-0001-8888-4493
Ke-Seng ZhaoGuangdong Provincial Key Lab of Shock and Microcirculation, Department of Pathophysiology, Southern Medical University, Guangzhou, 510515, China.
Qiaobing HuangGuangdong Provincial Key Lab of Shock and Microcirculation, Department of Pathophysiology, Southern Medical University, Guangzhou, 510515, China. bing@smu.edu.cn.
Zhongqing ChenDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. zhongqingchen2008@163.com.ORCID http://orcid.org/0000-0003-2482-949X
Nanfang Hospital · CNSouthern Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81170297National Natural Science Foundation of China (National Science Foundation of China) 81701955National Natural Science Foundation of China (National Science Foundation of China) 81703935National Natural Science Foundation of China (National Science Foundation of China) 81870210Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2016A030310389Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2016A030313561Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2017A030313590
6 · The paper itself

Abstract

In a previous study, we demonstrated the role of polydatin (PD) in protecting against multiple organ dysfunction in sepsis. The aim of this study is to investigate whether PD protects against lipopolysaccharide (LPS)-induced endothelial barrier disruption through SIRT3 activation and to disclose the underlying mechanisms. Wild-type mice were injected with LPS and Evans Blue assay was performed to evaluate vascular permeability. Primary human umbilical vein endothelial cells (HUVECs) were stimulated with LPS. Endothelial permeability was evaluated by transendothelial electrical resistance (TER) and FITC-dextran leakage. SIRT3 activity was determined by a Deacetylase Fluorometric kit, and protein expression level of SIRT3 was detected by western blotting. Mitochondrial function was evaluated by determination of ROS level, mitochondrial membrane potential and mPTP opening. In endotoxemic mice, PD pretreatment attenuated vascular leakage in multiple organs while SIRT3 inhibition with 3-TYP reversed the effects of PD. PD treatment in late sepsis also exhibited barrier protective effects. In HUVECs, PD alleviated LPS-induced F-actin rearrangement, cadherin-catenin complex dissociation and endothelial hyperpermeability, whereas 3-TYP or SIRT3 siRNA attenuated the protective effects of PD. PD enhanced SIRT3 deacetylase activity, and attenuated LPS-induced decrease in SIRT3 expression as well. Furthermore, gain-of-function and loss-of-function strategies also confirmed the role of SIRT3 in enhancing endothelial barrier integrity. It was further ascertained that PD enhanced SIRT3-mediated deacetylation of SOD2 and cyclophilin D (CypD), thus suppressing mitochondrial dysfunction and subsequent endothelial barrier dysfunction. In addition, it was revealed that RAGE was involved in LPS-regulated SIRT3 signaling. Our results suggest that polydatin protects against LPS-induced endothelial barrier disruption dependent on SIRT3 and can be applied as a potential therapy for sepsis.

Indexed as

AnimalsCapillary PermeabilityCells, CulturedEndothelium, VascularGlucosidesHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMiceProtective AgentsSignal TransductionSirtuin 3StilbenesGlucosidesLipopolysaccharidespolydatinProtective AgentsSirt3 protein, mouseSirtuin 3Stilbenes

Identifiers

PMID31641228
OpenAlexW2981836840

What OpenQuestion holds

Textmetadata
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.