Evidence map›Paper›PMID 34011327›Full record

ArticleBMC complementary medicine and therapies2021

Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy.

Lijiao You, Di Zhang, Huan Geng, Fangyuan Sun, Ming Lei

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

Article in BMC complementary medicine and therapies, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

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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 1 institution in 1 country.

Lijiao You *Department of Critical Care Medicine, Seventh People's Hospital of Shanghai University of TCM, No.358 Datong Road, Gaoqiao Town, Pudong New District, Shanghai, 200137, China.
Di Zhang *Department of Rehabilitation Medicine, Seventh People's Hospital of Shanghai University of TCM, Shanghai, 200137, P.R. China.
Huan GengDepartment of Critical Care Medicine, Seventh People's Hospital of Shanghai University of TCM, No.358 Datong Road, Gaoqiao Town, Pudong New District, Shanghai, 200137, China.
Fangyuan SunDepartment of Critical Care Medicine, Seventh People's Hospital of Shanghai University of TCM, No.358 Datong Road, Gaoqiao Town, Pudong New District, Shanghai, 200137, China.
Ming LeiDepartment of Critical Care Medicine, Seventh People's Hospital of Shanghai University of TCM, No.358 Datong Road, Gaoqiao Town, Pudong New District, Shanghai, 200137, China. leimsh@163.com.ORCID http://orcid.org/0000-0002-8099-7095
Shanghai University · CN

Funding

Health and Family Planning Committee of Pudong New Area (CN) PWR12019-02National Natural Science Foundation of China 81973649Talents Training Program of Seventh People's Hospital of Shanghai University of TCM XX2020-15The Outstanding Clinical Discipline Project of Shanghai Pudong PWYgy2018-01
6 · The paper itself

Abstract

backgroundSalidroside (SAL) is a bioactive compound extracted from Rhodiola rosea with various biological properties. This study was designed to explore the functions of SAL on the endothelial damage induced by lipopolysaccharide (LPS) and its related mechanisms.

methodsHuman umbilical vein endothelial cells (HUVECs) were pretreated with SAL (0, 10, 25, 50, 100 μM), and then incubated with LPS (10 μg/mL). Cell viability was evaluated by MTT assay, cell injury by lactate dehydrogenase (LDH) release, and inflammatory cytokines release by ELISA assay. Oxidative stress was evaluated by malondialdehyde (MDA) and superoxide dismutase (SOD) in cell lysate. Apoptosis was detected by flow cytometry and caspase-3 activity. Western blot were performed to determine expression levels of autophagy and NOD-like receptor protein 3 (NLRP3) related proteins.

resultsSAL at 50 μM concentration showed no toxicity on HUVECs, but attenuated LPS-induced injury, as evidenced by increased cell viability, reduction in LDH level and inflammatory cytokines in culture media. SAL also reduced MDA level and increased SOD activity in HUVECs, and inhibited apoptosis rate and caspase-3 activity. (P < 0.05). Moreover, LPS enhanced HUVECs autophagy, and SAL pretreatment further enhanced autophagy, with increased Beclin-1 protein and decreased P62 protein. SAL also attenuated LPS-induced activation of NLRP3 inflammasome, reduced the protein expression of NLRP3-related proteins, including ASC and caspase-1. Autophagy inhibition by 3-MA markedly reversed SAL-modulated changes in cell viability and NLRP3 expression in LPS-stimulated HUVECs.

conclusionSAL protects endothelial cells against LPS-induced injury through inhibition of NLRP3 pathways and enhancing autophagy.

Indexed as

InflammationApoptosisAutophagyCells, CulturedGlucosidesHumansHuman Umbilical Vein Endothelial CellsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinPhenolsSignal TransductionGlucosidesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanPhenolsrhodiolosideApoptosisAutophagyHuman umbilical vein endothelial cells (HUVECs)InflammationLipopolysaccharide (LPS)NOD-like receptor protein 3 (NLRP3)Salidroside (SAL)Sepsis

Identifiers

PMID34011327
PMCPMC8136193
OpenAlexW3163498352

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.