Evidence map›Paper›PMID 33981156›Full record

ArticleJournal of inflammation research2021

Dual Activity of Ginsenoside Rb1 in Hypertrophic Cardiomyocytes and Activated Macrophages: Implications for the Therapeutic Intervention of Cardiac Hypertrophy.

Shihua Wang, Yimeng Cui, Minqi Xiong, Mei Li, Peiwei Wang, Jingang Cui, Xiaoye Du, Yu Chen, Teng Zhang

Abstract read
In one paragraph

Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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, 2 syntheses or guidelines pooled it.

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  8. Ginsenoside RbChinese herbal medicines · 2024
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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

9 authors.

Shihua WangYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Yimeng CuiYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Minqi XiongYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Mei LiYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Peiwei WangYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Jingang CuiYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Xiaoye DuYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Yu ChenYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Teng ZhangYueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeOwing to the important mechanistic implications in the pathogenesis of cardiac hypertrophy and heart failure, inflammation has been proposed as a druggable target for the treatment of cardiac hypertrophy and heart failure. Ginseng is a widely used medicinal herb for the treatment of cardiovascular disorders. As one of the major chemical components of ginseng, ginsenoside Rb1 (Rb1) contributes to the cardiovascular effects of ginseng. Meanwhile, anti-inflammatory activity of Rb1 has also been documented. The current work aims to further delineate the pharmacological implications of Rb1 in the treatment of cardiac hypertrophy.

methodsAngiotensin II (Ang II) infusion mouse model was adopted to investigate the effects of Rb1 on cardiac hypertrophic remodeling and associated inflammation in vivo. Furthermore, the mechanisms of actions of Rb1 in modulating the hypertrophic and inflammatory responses were investigated in cardiomyocytes and macrophages, respectively.

resultsRb1 mitigates Ang II-induced cardiac hypertrophy, cardiac inflammation and systemic inflammation in vivo. In cardiomyocytes, Rb1 directly counteracts the pro-hypertrophic effects of Ang II and phenylephrine and maintains the mitochondrial function. In lipopolysaccharide (LPS)-stimulated macrophages, Rb1 decreases the phosphorylation of mitogen-activated protein kinases (MAPKs) and mitogen-activated protein kinase kinase 1/2 (MEK1/2) and reduces the production of inflammation mediators such as interleukin (IL)-1 beta, IL-6 and tumor necrosis factor (TNF). Rb1 also suppresses the expression of pro-hypertrophic microRNA-155 (miR-155) in LPS- or Ang II-stimulated macrophages. Furthermore, in activated macrophages, miR-155 is in part accountable for the suppressive effect of Rb1 on the production of IL-6, an inflammation mediator with pro-hypertrophic functions in the heart.

conclusionThe work here provides novel experimental evidence supporting the notion that Rb1 protects against cardiac hypertrophy in part through suppressing the inflammatory mechanisms that promotes the pathological remodeling of the heart.

Indexed as

angiotensin IIinflammationinterleukin 6

Identifiers

PMID33981156
PMCPMC8108398

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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 OpenQuestion graph.