Evidence map›Paper›PMID 35986876›Full record

ArticleNeurotoxicity research2022

Polydatin Prevents Neuroinflammation and Relieves Depression via Regulating Sirt1/HMGB1/NF-κB Signaling in Mice.

Hetao Bian, Ling Xiao, Liang Liang, Yinping Xie, Huiling Wang, Mark Slevin, Wen-Jun Tu, Gaohua Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026
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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

8 authors at 4 institutions in 2 countries.

Hetao BianDepartment of Psychiatry, Renmin Hospital of Wuhan University, Jiefang Road 238#, 430060, Hubei, People's Republic of China.
Ling XiaoDepartment of Psychiatry, Renmin Hospital of Wuhan University, Jiefang Road 238#, 430060, Hubei, People's Republic of China.
Liang LiangDepartment of Psychiatry, Renmin Hospital of Wuhan University, Jiefang Road 238#, 430060, Hubei, People's Republic of China.
Yinping XieDepartment of Psychiatry, Renmin Hospital of Wuhan University, Jiefang Road 238#, 430060, Hubei, People's Republic of China.
Huiling WangDepartment of Psychiatry, Renmin Hospital of Wuhan University, Jiefang Road 238#, 430060, Hubei, People's Republic of China.
Mark SlevinSchool of Healthcare Science, Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, M156GX, UK. M.A.Slevin@mmu.ac.uk.
Wen-Jun TuInstitute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, No. 238, Baiti Road, Tianjin, 300192, People's Republic of China. tuwenjun@irm-cams.ac.cn.
Gaohua WangDepartment of Psychiatry, Renmin Hospital of Wuhan University, Jiefang Road 238#, 430060, Hubei, People's Republic of China. wgh6402@163.com.
Renmin Hospital of Wuhan University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNManchester Metropolitan University · GBWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depression is a prevalent psychiatric disorder with a significant health impact and economic burden worldwide. Unfortunately, the exact pathogenesis of depression is not well understood. Neuroinflammation and microglial activation play an essential role in the pathogenesis of depression. Previous studies have shown that polydatin has anti-inflammatory and antioxidant properties. However, the link between polydatin and depression remains unclear. Therefore, the objective of this study was to investigate the antidepressant effect of polydatin in lipopolysaccharide (LPS)-induced depression in mice and its possible mechanism. Adult male C57BL/6 J mice were used in this study. The polydatin and LPS were injected intraperitoneally daily for 5 days. In addition, the EX527, an inhibitor of Sirt1, was injected intraperitoneally daily and 1 h before the polydatin injection. The behavior tests were performed to elucidate the depression-like behaviors. The Sirt1/HMGB1/NF-κB pathway expression was detected by western blot, ELISA, and immunofluorescence staining. Polydatin can significantly improve LPS-induced depression-like behavior in mice. Treatment with polydatin increased the expression of the Sirt1 but decreased the expression of the HMGB1, p-NF-κB, IL-1b, and TNF-α in the LPS-induced depression mice. In addition, the EX527 abolished the anti-depressive effects of the polydatin and the levels of Sirt1 protein. These findings suggested that the polydatin reversed the depressive effects through the Sirt1/HMGB1/NF-κB signaling in the LPS-induced depression mice. Therefore, polydatin can be used in the treatment of depression.

Indexed as

HMGB1 ProteinNF-kappa BAnimalsAntidepressive AgentsAnti-Inflammatory AgentsAntioxidantsDepressionGlucosidesHumansLipopolysaccharidesMaleMiceMice, Inbred C57BLNeuroinflammatory DiseasesSirtuin 1StilbenesAntidepressive AgentsAnti-Inflammatory AgentsAntioxidantsGlucosidesHMGB1 ProteinLipopolysaccharidesNF-kappa BpolydatinSIRT1 protein, humanSirt1 protein, mouseSirtuin 1StilbenesTumor Necrosis Factor-alphaDepressionLipopolysaccharideNeuroinflammationPolydatinsirt1

Identifiers

PMID35986876
OpenAlexW4292549403

What Socratic 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 Socratic graph.