Evidence map›Paper›PMID 27517893›Full record

ArticleMolecules (Basel, Switzerland)2016

Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway.

Yao Zhu, Ya-Jie Zhang, Wei-Wei Liu, Ai-Wu Shi, Ning Gu

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.5field-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

40 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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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

5 authors at 3 institutions in 1 country.

Yao ZhuFirst College of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China. zy_njtcm@126.com.
Ya-Jie ZhangNanjing Hospital of Traditional Chinese Medicine, Nanjing 210001, China. zhangyajie_jack@126.com.
Wei-Wei LiuFirst College of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China. cheeseweiweiliu@126.com.
Ai-Wu ShiNanjing Maternity and Child Health Care Hospital, Nanjing 210004, China. shiaiwu888@163.com.
Ning GuNanjing Hospital of Traditional Chinese Medicine, Nanjing 210001, China. jsguning@163.com.
Nanjing Traditional Chinese Medicine Hospital · CNNanjing University · CNNanjing Maternity and Child Health Care Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Salidroside (SAL), one of the main effective constituents of Rhodiola rosea, has been reported to suppress oxidative stress-induced cardiomyocyte injury and necrosis by promoting transcription of nuclear factor E2-related factor 2 (Nrf2)-regulated genes such as heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase (quinone1) (NQO1). However, it has not been indicated whether SAL might ameliorate endothelial injury induced by oxidative stress. Here, our study demonstrated that SAL might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway. The results of our study indicated that SAL decreased the levels of intercellular reactive oxygen species (ROS) and malondialdehyde (MDA), and improved the activities of superoxide dismutase (SOD) and catalase (CAT), resulting in protective effects against oxidative stress-induced cell damage in HUVECs. It suppressed oxidative stress damage by inducing Nrf2 nuclear translocation and activating the expression of Nrf2-regulated antioxidant enzyme genes such as HO-1 and NQO1 in HUVECs. Knockdown of Nrf2 with siRNA abolished the cytoprotective effects against oxidative stress, decreased the expression of Nrf2, HO-1, and NQO1, and inhibited the nucleus translocation of Nrf2 in HUVECs. This study is the first to demonstrate that SAL suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.

Indexed as

CatalaseGlucosidesHeme Oxygenase-1Human Umbilical Vein Endothelial CellsMalondialdehydeNAD(P)H Dehydrogenase (Quinone)NF-E2-Related Factor 2Oxidative StressPhenolsReactive Oxygen SpeciesSignal TransductionSuperoxide DismutaseCatalaseGlucosidesHeme Oxygenase-1HMOX1 protein, humanMalondialdehydeNAD(P)H Dehydrogenase (Quinone)NFE2L2 protein, humanNF-E2-Related Factor 2NQO1 protein, humanPhenolsReactive Oxygen SpeciesrhodiolosideSuperoxide Dismutaseheme oxygenase-1human umbilical vein endothelial cellsNAD(P)H dehydrogenase (quinone1)nuclear factor E2-related factor 2oxidative stresssalidroside

Identifiers

PMID27517893
PMCPMC6273208
OpenAlexW2479133488

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.