Evidence map›Paper›PMID 24908654›Full record

ArticleJournal of lipid research2014

Rutaecarpine suppresses atherosclerosis in ApoE-/- mice through upregulating ABCA1 and SR-BI within RCT.

Yanni Xu, Qi Liu, Yang Xu, Chang Liu, Xiao Wang, Xiaobo He, Ningyu Zhu, Jikai Liu, Yexiang Wu, Yongzhen Li and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 67 citations in OpenAlex.

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  11. Pharmacological blockage of the AHR-CYP1A1 axis: a call for in vivo evidence.Journal of molecular medicine (Berlin, Germany) · 2022
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  19. Identification ofRSC medicinal chemistry · 2020
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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

17 authors at 2 institutions in 1 country.

Yanni XuInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Qi LiuInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Yang XuInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Chang LiuInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Xiao WangInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Xiaobo HeInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Ningyu ZhuInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Jikai LiuInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Yexiang WuInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Yongzhen LiInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Ni LiInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Tingting FengInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Fangfang LaiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Murui ZhangSir Runrun Shaw Hospital of Zhejiang University, Hangzhou, Zhejiang Province 310016, China.
Bin HongInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Jian-Dong JiangInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Shuyi SiInstitute of Medicinal Biotechnology Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ABCA1 and scavenger receptor class B type I (SR-BI)/CD36 and lysosomal integral membrane protein II analogous 1 (CLA-1) are the key transporter and receptor in reverse cholesterol transport (RCT). Increasing the expression level of ABCA1 and SR-BI/CLA-1 is antiatherogenic. The aim of the study was to find novel antiatherosclerotic agents upregulating expression of ABCA1 and SR-BI/CLA-1 from natural compounds. Using the ABCA1p-LUC and CLA-1p-LUC HepG2 cell lines, we found that rutaecarpine (RUT) triggered promoters of ABCA1 and CLA-1 genes. RUT increased ABCA1 and SR-BI/CLA-1 expression in vitro related to liver X receptor alpha and liver X receptor beta. RUT induced cholesterol efflux in RAW264.7 cells. ApoE-deficient (ApoE(-/-)) mice treated with RUT for 8 weeks showed ∼68.43, 70.23, and 85.56% less en face lesions for RUT (L), RUT (M), and RUT (H) groups, respectively, compared with the model group. Mouse macrophage-specific antibody and filipin staining indicated that RUT attenuated macrophages and cholesterol accumulations in atherosclerotic lesions, respectively. Additionally, ABCA1 and SR-BI expression was highly induced by RUT in livers of ApoE(-/-) mice. Meanwhile, RUT treatment significantly increased the fecal (3)H-cholesterol excretion, which demonstrated that RUT could promote RCT in vivo. RUT was identified to be a candidate that protected ApoE(-/-) mice from developing atherosclerosis through preferentially promoting activities of ABCA1 and SR-BI within RCT.

Indexed as

AnimalsApolipoproteins EAtherosclerosisATP Binding Cassette Transporter 1Indole AlkaloidsLiverMiceMice, KnockoutQuinazolinesQuinazolinonesRAW 264.7 CellsScavenger Receptors, Class BABCA1 protein, humanAbca1 protein, mouseApolipoproteins EATP Binding Cassette Transporter 1Indole AlkaloidsQuinazolinesQuinazolinonesrutecarpineSCARB1 protein, humanScarb1 protein, mouseScavenger Receptors, Class Bapolipoprotein E deficientATP binding cassette transporter A1reverse cholesterol transportscavenger receptor class B type I

Identifiers

PMID24908654
PMCPMC4109758
OpenAlexW2087906616

What OpenQuestion holds

Textmetadata
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.