Evidence map›Paper›PMID 30227623›Full record

ArticleMolecules (Basel, Switzerland)2018

RhoA/ROCK-2 Pathway Inhibition and Tight Junction Protein Upregulation by Catalpol Suppresses Lipopolysaccaride-Induced Disruption of Blood-Brain Barrier Permeability.

Shan Feng, Li Zou, Hongjin Wang, Ran He, Ke Liu, Huifeng Zhu

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

71 citing papers in PubMed, 122 citations in OpenAlex.

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  9. The Eph-ephrin system in neuropsychiatric and neurodevelopmental disorders.Journal of psychiatry & neuroscience : JPN · 2026
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11 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Shan FengCollege of Pharmaceutical Sciences and Chinese Medicine, Southwest University, 2# Tiansheng Road, Beibei District, Chongqing 400715, China. fengshan@swu.edu.cn.
Li ZouCollege of Pharmaceutical Sciences and Chinese Medicine, Southwest University, 2# Tiansheng Road, Beibei District, Chongqing 400715, China. zxm18611@163.com.
Hongjin WangCollege of Pharmaceutical Sciences and Chinese Medicine, Southwest University, 2# Tiansheng Road, Beibei District, Chongqing 400715, China. wanghongjin0105@outlook.com.
Ran HeCollege of Pharmaceutical Sciences and Chinese Medicine, Southwest University, 2# Tiansheng Road, Beibei District, Chongqing 400715, China. hr606@swu.edu.cn.
Ke LiuCollege of Pharmaceutical Sciences and Chinese Medicine, Southwest University, 2# Tiansheng Road, Beibei District, Chongqing 400715, China. liuke1030@126.com.
Huifeng ZhuCollege of Pharmaceutical Sciences and Chinese Medicine, Southwest University, 2# Tiansheng Road, Beibei District, Chongqing 400715, China. zhfbsci@126.com.ORCID 0000-0003-3927-5151
Southwest University · CN

Funding

China Postdoctoral Science Foundation 2016M602641Chongqing Research Program Basic Research and Frontier Technology cstc2017jcyjAX0137National Natural Science Foundation of China 81402393National Natural Science Foundation of China 81572678Postdoctoral Foundation of Southwest University 102060-20750902
6 · The paper itself

Abstract

Lipopolysaccaride (LPS) directly or indirectly injures brain microvascular endothelial cells (BMECs) and damages the intercellular tight junction that gives rise to altered blood-brain barrier (BBB) permeability. Catalpol plays a protective role in LPS-induced injury, but whether catalpol protects against LPS-caused damage of BBB permeability and the underlying mechanism remain to be delineated. Prophylactic protection with catalpol (5 mg/kg, i.v.) consecutively for three days reversed the LPS-induced damage of BBB by decreased Evans Blue (EB) leakage and restored tight junctions in C57 mice. Besides, catalpol co-administrated with LPS increased BMECs survival, decreased their endothelin-1, TNF-Α and IL-6 secretion, improved transmembrane electrical resistance in a time-dependent manner, and in addition increased the fluorescein sodium permeability coefficient of BMECs. Also, transmission electron microscopy showed catalpol protective effects on tight junctions. Fluorescence staining displayed that catalpol reversed the rearrangement of the cytoskeleton protein F-actin and upregulated the tight junction protein of claudin-5 and ZO-1, which have been further demonstrated by the mRNA and protein expression levels of ZO-1, ZO-2, ZO-3, claudin-5, and occludin. Moreover, catalpol concurrently downregulated the mRNA and protein levels of RhoA, and ROCK2, the critical proteins in the RhoA/ROCK2 signaling pathway. This study thus indicated that catalpol, via inhibition of the RhoA/ROCK2 signaling pathway, reverses the disaggregation of cytoskeleton actin in BMECs and prevents down-regulation of junctional proteins, such as claudin-5, occludin, and ZO-1, and decreases endothelin-1 and inflammatory cytokine secretion, eventually alleviating the increase in LPS-induced BBB permeability.

Indexed as

Signal TransductionUp-RegulationActinsAnimalsBlood-Brain BarrierCell SurvivalClaudin-5Down-RegulationElectric ImpedanceEndothelial CellsIridoid GlucosidesLipopolysaccharidesMaleMice, Inbred C57BLOccludinPermeabilityActinscatalpolClaudin-5Iridoid GlucosidesLipopolysaccharidesOccludinProtective AgentsrhoA GTP-Binding Proteinrho-Associated KinasesTight Junction ProteinsZonula Occludens-1 ProteinBBBcatalpolLPSRhoA/ROCK2tight junction

Identifiers

PMID30227623
PMCPMC6225311
OpenAlexW2889675398

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.