Evidence map›Paper›PMID 29925377›Full record

ArticleJournal of neuroinflammation2018

Vitexin reduces epilepsy after hypoxic ischemia in the neonatal brain via inhibition of NKCC1.

Wen-di Luo, Jia-Wei Min, Wen-Xian Huang, Xin Wang, Yuan-Yuan Peng, Song Han, Jun Yin, Wan-Hong Liu, Xiao-Hua He, Bi-Wen Peng

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.1field-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

23 citing papers in PubMed, 45 citations in OpenAlex.

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  13. Blood-CNS barrier dysfunction in amyotrophic lateral sclerosis: Proposed mechanisms and clinical implications.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
  14. Review
  15. Article
  16. Anti-Inflammatory Effects of Phytochemical Components ofMolecules (Basel, Switzerland) · 2022
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  18. Article
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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

10 authors at 1 institution in 1 country.

Wen-di LuoDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University, Hubei Donghu Rd 185#, Wuhan, 430071, Hubei, China.
Jia-Wei MinDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University, Hubei Donghu Rd 185#, Wuhan, 430071, Hubei, China.
Wen-Xian HuangDepartment of Pathology, Renmin Hospital, Wuhan University, Wuhan, China.
Xin WangDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University, Hubei Donghu Rd 185#, Wuhan, 430071, Hubei, China.
Yuan-Yuan PengDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University, Hubei Donghu Rd 185#, Wuhan, 430071, Hubei, China.
Song HanDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Jun YinDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Wan-Hong LiuDepartment of Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Xiao-Hua HeDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Bi-Wen PengDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University, Hubei Donghu Rd 185#, Wuhan, 430071, Hubei, China. pengbiwen@whu.edu.cn.ORCID http://orcid.org/0000-0002-5599-6779
Wuhan University · CN

Funding

Independent Scientific Research Project Fund of Wuhan University 2042017kt0066National Natural Science Foundation of China 81370737National Natural Science Foundation of China 81571481National Natural Science Foundation of China 81601325
6 · The paper itself

Abstract

backgroundNeonatal hypoxic-ischemic brain damage, characterized by tissue loss and neurologic dysfunction, is a leading cause of mortality and a devastating disease of the central nervous system. We have previously shown that vitexin has been attributed various medicinal properties and has been demonstrated to have neuroprotective roles in neonatal brain injury models. In the present study, we continued to reinforce and validate the basic understanding of vitexin (45 mg/kg) as a potential treatment for epilepsy and explored its possible underlying mechanisms.

methodsP7 Sprague-Dawley (SD) rats that underwent right common carotid artery ligation and rat brain microvascular endothelial cells (RBMECs) were used for the assessment of Na

resultsOur data showed that NKCC1 expression was attenuated in vitexin-treated rats compared to the expression in the HI group in vivo. Oxygen glucose deprivation/reoxygenation (OGD) was performed on RBMECs to explore the role of NKCC1 and F-actin in cytoskeleton formation with confocal microscopy, N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide, and FCM. Concomitantly, treatment with vitexin effectively alleviated OGD-induced NKCC1 expression, which downregulated F-actin expression in RBMECs. In addition, vitexin significantly ameliorated BBB leakage and rescued the expression of tight junction-related protein ZO-1. Furthermore, inflammatory cytokine and neutrophil infiltration were concurrently and progressively downregulated with decreasing BBB permeability in rats. Vitexin also significantly suppressed brain electrical activity in neonatal rats.

conclusionsTaken together, these results confirmed that vitexin effectively alleviates epilepsy susceptibility through inhibition of inflammation along with improved BBB integrity. Our study provides a strong rationale for the further development of vitexin as a promising therapeutic candidate treatment for epilepsy in the immature brain.

Indexed as

AnimalsAnimals, NewbornAnticonvulsantsApigeninCell HypoxiaCells, CulturedChloridesCytokinesDisease Models, AnimalEndothelial CellsEpilepsyGene Expression RegulationGlucoseGranulocyte Colony-Stimulating FactorHypoxia-Ischemia, BrainInterleukin-3AnticonvulsantsApigeninChloridesCytokinesGlucoseGranulocyte Colony-Stimulating FactorInterleukin-3myelopoietinNerve Tissue ProteinsRecombinant Fusion ProteinsSolute Carrier Family 12, Member 2Tjp1 protein, ratvitexinZonula Occludens-1 ProteinBlood-brain barrierEpilepsyF-actinHIBDInflammationNKCC1Vitexin

Identifiers

PMID29925377
PMCPMC6011387
OpenAlexW2809569263

What Socratic 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 Socratic graph.