Evidence map›Paper›PMID 24868319›Full record

ArticleOxidative medicine and cellular longevity2014

Salidroside stimulates mitochondrial biogenesis and protects against H₂O₂-induced endothelial dysfunction.

Shasha Xing, Xiaoyan Yang, Wenjing Li, Fang Bian, Dan Wu, Jiangyang Chi, Gao Xu, Yonghui Zhang, Si Jin

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Efficacy and safety of three species ofFrontiers in pharmacology · 2023
    Pooled it
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  18. Antioxidant Effects of Salidroside in the Cardiovascular System.Evidence-based complementary and alternative medicine : eCAM · 2020
    Review
  19. 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

9 authors at 1 institution in 1 country.

Shasha XingDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Xiaoyan YangDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Wenjing LiDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Fang BianDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Dan WuDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Jiangyang ChiDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Gao XuDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Yonghui ZhangDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Si JinDepartment of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; The Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation of Hubei Province, Wuhan 430030, China.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Salidroside (SAL) is an active component of Rhodiola rosea with documented antioxidative properties. The purpose of this study is to explore the mechanism of the protective effect of SAL on hydrogen peroxide- (H2O2-) induced endothelial dysfunction. Pretreatment of the human umbilical vein endothelial cells (HUVECs) with SAL significantly reduced the cytotoxicity brought by H2O2. Functional studies on the rat aortas found that SAL rescued the endothelium-dependent relaxation and reduced superoxide anion (O2(∙-)) production induced by H2O2. Meanwhile, SAL pretreatment inhibited H2O2-induced nitric oxide (NO) production. The underlying mechanisms involve the inhibition of H2O2-induced activation of endothelial nitric oxide synthase (eNOS), adenosine monophosphate-activated protein kinase (AMPK), and Akt, as well as the redox sensitive transcription factor, NF-kappa B (NF- κ B). SAL also increased mitochondrial mass and upregulated the mitochondrial biogenesis factors, peroxisome proliferator-activated receptor gamma-coactivator-1alpha (PGC-1 α ), and mitochondrial transcription factor A (TFAM) in the endothelial cells. H2O2-induced mitochondrial dysfunction, as demonstrated by reduced mitochondrial membrane potential (Δ ψ m) and ATP production, was rescued by SAL pretreatment. Taken together, these findings implicate that SAL could protect endothelium against H2O2-induced injury via promoting mitochondrial biogenesis and function, thus preventing the overactivation of oxidative stress-related downstream signaling pathways.

Indexed as

AMP-Activated Protein KinasesAnimalsAortaCells, CulturedCell SurvivalGlucosidesHumansHuman Umbilical Vein Endothelial CellsHydrogen PeroxideMitochondriaNF-kappa BNitric Oxide Synthase Type IIIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhenolsProto-Oncogene Proteins c-aktRatsAMP-Activated Protein KinasesGlucosidesHydrogen PeroxideNF-kappa BNitric Oxide Synthase Type IIIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhenolsPpargc1a protein, ratProto-Oncogene Proteins c-aktrhodiolosideTranscription Factors

Identifiers

PMID24868319
PMCPMC4020198
OpenAlexW2102211293

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.