Evidence map›Paper›PMID 28983639›Full record

ArticleHerz2019

Ginsenoside-Rb3 inhibits endothelial-mesenchymal transition of cardiac microvascular endothelial cells.

L Yang, Q Liu, Y Yu, H Xu, S Chen, S Shi

Abstract read
PubMed Publisher
In one paragraph

Article in Herz, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  3. Review
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  6. 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

6 authors at 1 institution in 1 country.

L YangThe First Affiliated Hospital of Zhejiang Traditional Chinese Medicine University, 310053, Hangzhou, China.
Q LiuThe First Affiliated Hospital of Zhejiang Traditional Chinese Medicine University, 310053, Hangzhou, China. 13588121905@163.com.
Y YuThe First Affiliated Hospital of Zhejiang Traditional Chinese Medicine University, 310053, Hangzhou, China.
H XuThe First Affiliated Hospital of Zhejiang Traditional Chinese Medicine University, 310053, Hangzhou, China.
S ChenThe First Affiliated Hospital of Zhejiang Traditional Chinese Medicine University, 310053, Hangzhou, China.
S ShiCollege of Pharmacy, Zhejiang Traditional Chinese Medicine University, 310053, Hangzhou, China.
Zhejiang Chinese Medical University · CN

Funding

the Natural Science Fund of ZheJiang Province in China LY13H270013
6 · The paper itself

Abstract

backgroundWe investigated the effect of Ginsenoside-Rb3 (Rb3) on the endothelial-to-mesenchymal transition (EMT) of cardiac microvascular endothelial cells (CMVECs) following coxsackievirus B3 (CVB3) infection.

methodsCMVECs were infected with 100 TCID50 CVB3 (CVB3 group) or treated with Rb3 (Rb3 group); stably cultured CMVECs were used as control. Cells treated with the Pyk2 inhibitor TAE226 and PI3K inhibitor LY294002 were used for additional experiments. Cell viability was assessed with the Cell Counting Kit-8 (CCK8). Expression of CD31 and α‑smooth muscle actin (α-SMA) was evaluated by immunofluorescence (IF) and Western blotting (WB). Expression of Pyk2, PI3K, and AKT was assessed by real-time polymerase chain reaction (RT-PCR) and WB.

resultsCell morphology, including cell pyknosis, and viability were significantly impaired by CVB3 infection (p < 0.05). However, the morphology of the Rb3 group was unaffected. The CCK8 assay showed that viability in the Rb3 group was increased compared with the CVB3 group (p < 0.05). Expression of CD31 decreased and α‑SMA increased in the CVB3 group compared with the control group (p < 0.05), but CD31 increased while α‑SMA decreased in the Rb3 group compared with the CVB3 group (p < 0.05). IF staining showed the same trends. The levels of Pyk2, PI3K, AKT, and CD31 were up-regulated in the Rb3 group compared with the CVB3 group, whereas α‑SMA decreased (p < 0.05). In the Pyk2-inhibitor group, PI3K, AKT, and CD31 expression was down-regulated while α‑SMA expression increased in comparison with the Rb3 group (p < 0.05). In the PI3K-inhibitor group, the levels of AKT and CD31 decreased while α‑SMA increased (p < 0.05), although the level of Pyk2 expression showed no obvious change in comparison with the Rb3 group.

conclusionRb3 inhibited EMT in CMVECs following CVB3 infection via the Pyk2-PI3K-AKT signaling pathway.

Indexed as

Coxsackievirus InfectionsGinsenosidesMyocarditisEndothelial CellsHumansPhosphatidylinositol 3-KinasesSignal Transductionginsenoside Rb3GinsenosidesPhosphatidylinositol 3-KinasesCoxsackievirus infectionsEndomyocardial fibrosisGinsenosidesMyocarditisSignal pathways

Identifiers

PMID28983639
OpenAlexW2762040868

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.