Evidence map›Paper›PMID 28824425›Full record

ArticleFrontiers in pharmacology2017

Attenuation of TNF-α-Induced Inflammatory Injury in Endothelial Cells by Ginsenoside Rb1 via Inhibiting NF-κB, JNK and p38 Signaling Pathways.

Ping Zhou, Shan Lu, Yun Luo, Shan Wang, Ke Yang, Yadong Zhai, Guibo Sun, Xiaobo Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Ginseng and health outcomes: an umbrella review.Frontiers in pharmacology · 2023
    Pooled it
  2. Review
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  18. Ginsenoside RbChinese herbal medicines · 2024
    Review
  19. Neutrophil Extracellular Traps Affect Human Inner Ear Vascular Permeability.International journal of molecular sciences · 2024
    Article
  20. Article

27 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

8 authors at 3 institutions in 1 country.

Ping ZhouInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Shan LuInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Yun LuoInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Shan WangInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Ke YangInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Yadong ZhaiInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Guibo SunInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Xiaobo SunInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical SciencesBeijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNMinistry of Education of the People's Republic of China · CNState Administration of Traditional Chinese Medicine of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is currently believed that inflammation plays a central role in the pathophysiology of atherosclerosis. Oxidative stress and redox-sensitive transcription factors are implicated in the process. Ginsenoside Rb1, a major active ingredient in processed Radix notoginseng, has attracted widespread attention because of its potential to improve cardiovascular function. However, the effects of ginsenoside Rb1 on tumor necrosis factor-α (TNF-α)-induced vascular endothelial cell injury and the underlying molecular mechanisms have never been studied. This study showed that TNF-α-induced oxidative stress, inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs) could be attenuated by ginsenoside Rb1 pretreatment. Using JC-1, Annexin V/PI and TUNEL staining, and a caspase-3 activity assay, we found that Rb1 provided significant protection against TNF-α-induced cell death. Furthermore, Rb1 pretreatment could inhibit TNF-α-induced ROS and MDA production; increase the activities of SOD, CAT, and GSH-Px; and decrease the levels of IL-1β, IL-6, VCAM-1, ICAM-1, VEGF, MMP-2 and MMP-9. Importantly, the cytoprotective effects of Rb1 were correlated with NF-κB signaling pathway inhibition. Additionally, we found that Rb1 may suppress the NF-κB pathway through p-38 and JNK pathway activation, findings supported by the results of our experiments involving anisomycin (AM), a JNK and p38 activator. In conclusion, this study showed that ginsenoside Rb1 protects HUVECs from TNF-α-induced oxidative stress and inflammation by inhibiting JNK and p38. This inhibition suppressed NF-κB signaling and down-regulated the expression of inflammatory factors and apoptosis-related proteins.

Indexed as

apoptosisatherosclerosisginsenoside Rb1inflammationtumor necrosis factor-α

Identifiers

PMID28824425
PMCPMC5540891
OpenAlexW2741524999

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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 OpenQuestion graph.