Evidence map›Paper›PMID 28098903›Full record

ArticleMolecular medicine reports2017

Vitexin alleviates lipopolysaccharide‑induced islet cell injury by inhibiting HMGB1 release.

Feifei Wang, Jiajing Yin, Yujin Ma, Hongwei Jiang, Yanbo Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  6. Anti-Inflammatory Effects of Phytochemical Components ofMolecules (Basel, Switzerland) · 2022
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  9. Comparison of the Effects of Intraperitoneal Injection with Carbon Tetrachloride on Acute Liver Toxicity in Male and Female Kunming Mice.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
  10. Article
  11. Review
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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 3 institutions in 1 country.

Feifei WangDepartment of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Jiajing YinDepartment of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Yujin MaDepartment of Endocrinology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Hongwei JiangDepartment of Endocrinology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Yanbo LiDepartment of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
First Affiliated Hospital of Harbin Medical University · CNFirst Affiliated Hospital of Henan University of Science and Technology · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) is a chronic metabolic disease, where the predominant pathogenesis is pancreatic β‑cells dysfunction or injury. It has been well established that inflammation leads to a gradual exhaustion of pancreatic β‑cell function with decreased β‑cell mass likely resulting from pancreatic β‑cells apoptosis or death. Vitexin, a major bioactive flavonoid compound in plants has numerous pharmacological properties, including antioxidant, anti‑inflammatory and antimyeloperoxidase. Whether vitexin can protect pancreatic β‑cells against lipopolysaccharide (LPS)‑induced pro‑inflammatory cytokine production and apoptosis has received little attention. The present study investigated the potential effects of vitexin on LPS‑induced pancreatic β‑cell injury and apoptosis. It was revealed that apoptosis and damage induced by LPS in islet tissue of rats and INS‑1 cells was significantly decreased in response to vitexin treatment. In addition, pretreatment with vitexin decreased the levels of the pro‑inflammatory cytokines tumor necrosis factor‑α and high mobility group box 1 (HMGB1) in LPS‑induced rats. Further experiments demonstrated that vitexin pretreatment suppressed the activation of P38 mitogen‑activated protein kinase signaling pathways in LPS‑induced INS‑1 cells. In conclusion, the results indicated that vitexin prevented LPS‑induced islet tissue damage in rats, and INS‑1 cells injury and apoptosis by inhibiting HMGB1 release. Therefore, the present study provided clear evidence indicating that vitexin may be a viable therapeutic strategy for the treatment of DM.

Indexed as

AnimalsApigeninApoptosisCell LineCell SurvivalHMGB1 ProteinImmunohistochemistryIslets of LangerhansLipopolysaccharidesMAP Kinase Signaling SystemProtective AgentsRatsApigeninHMGB1 ProteinLipopolysaccharidesProtective Agentsvitexin

Identifiers

PMID28098903
PMCPMC5367348
OpenAlexW2575031573

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.