Evidence map›Paper›PMID 31146723›Full record

ArticleBMC complementary and alternative medicine2019

Salidroside protects against ox-LDL-induced endothelial injury by enhancing autophagy mediated by SIRT1-FoxO1 pathway.

Zhongsheng Zhu, Jinyu Li, Xiaorong Zhang

Open access · goldAbstract read
In one paragraph

Article in BMC complementary and alternative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. StandardizedFrontiers in pharmacology · 2025
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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

3 authors at 1 institution in 1 country.

Zhongsheng ZhuDepartment of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, No.2800 Gongwei Road, Pudong New District, Shanghai, 201399, China. zhuzssh@163.com.ORCID http://orcid.org/0000-0002-8734-4214
Jinyu LiDepartment of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, No.2800 Gongwei Road, Pudong New District, Shanghai, 201399, China.
Xiaorong ZhangDepartment of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, No.2800 Gongwei Road, Pudong New District, Shanghai, 201399, China.
Fudan University · CN

Funding

Key Specialty Construction Project of Pudong New District of Shanghai PWZzk2017-17
6 · The paper itself

Abstract

backgroundAtherosclerosis is a condition with the vascular accumulation of lipid plaques, and its main major contributing factor is endothelial injury induced by oxidized low-density lipoprotein (ox-LDL). Salidroside (SAL) is the primary active ingredient of Rhodiola rosea, and exhibits antioxidant properties on endothelial cells and alleviates atherosclerosis. However, the effect of SAL on autophagy in ox-LDL-induced vascular endothelial injury remains unclear. Here, we investigated the effect and underlying mechanisms of SAL on autophagy in human umbilical vein endothelial cells (HUVECs).

methodsHUVECs were incubated with ox-LDL to induce in vitro atherosclerosis model. The cell viability and injury were evaluated by cell counting kit-8 (CCK-8) assay and lactate dehydrogenase (LDH) release assay. The oxidative stress was evaluated by NADPH oxidase, malondialdehyde (MDA) and superoxide dismutase (SOD) activities. Immunofluorescence was performed to detect autophagy using LC3β antibody. Quantitative real-time PCR (qRT-PCR) and western blot were performed to measure the mRNA expressions of SIRT1 and Forkhead box O1 (FOXO1). Nicotinamide (NAM) and AS1842856 were used to inhibit activities of SIRT1 and FOXO1, respectively.

resultsExposure of HUVECs to ox-LDL (100 μg/mL) reduced cell viability, increased cellular MDA, and reduced SOD in a concentration-dependent manner. The pretreatment with SAL (20, 50 and 100 μM) significantly enhanced the cell viability and decreased LDH release in HUVECs exposed to ox-LDL (100 μg/mL). ox-LDL induced autophagy in HUVECs, which was further enhanced by pretreatment with SAL. However, SAL attenuated increase in oxidative stress in HUVECs induced by ox-LDL. ox-LDL reduced mRNA and protein expressions of SIRT1 and FOXO1, which could be reversed by SAL. The protective, anti-oxidative and pro-autophagic effects of SAL could be obviously abolished by cotreatment with SIRT1 inhibitor or FOXO1 inhibitor.

conclusionSalidroside shows protective effect on endothelial cell induced by ox-LDL, and the mechanisms might be related to autophagy induction via increasing SIRT1 and FoxO1 expressions.

Indexed as

RhodiolaAtherosclerosisAutophagyDrug Evaluation, PreclinicalEndothelial CellsForkhead Box Protein O1GlucosidesHumansHuman Umbilical Vein Endothelial CellsLipoproteins, LDLOxidative StressPhenolsPhytotherapyPlant ExtractsSirtuin 1Forkhead Box Protein O1FOXO1 protein, humanGlucosidesLipoproteins, LDLoxidized low density lipoproteinPhenolsPlant ExtractsrhodiolosideSIRT1 protein, humanSirtuin 1AtherosclerosisAutophagyEndothelial cellOxidative stressOxidized low-density lipoprotein (ox-LDL)Salidroside (SAL)

Identifiers

PMID31146723
PMCPMC6543685
OpenAlexW2946853760

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.