Evidence map›Paper›PMID 27088510›Full record

ArticlePloS one2016

Hydroxysafflor Yellow A Ameliorates Renal Fibrosis by Suppressing TGF-β1-Induced Epithelial-to-Mesenchymal Transition.

Naping Hu, Jialin Duan, Huihui Li, Yanhua Wang, Fang Wang, Jianjie Chu, Jin Sun, Meiyou Liu, Chao Wang, Chengtao Lu and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
2.8field-weighted citation impact, top 9% 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, 37 citations in OpenAlex.

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  8. Hydroxysafflor Yellow A Blocks HIF-1Antioxidants (Basel, Switzerland) · 2022
    Article
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  20. Hydroxysafflor Yellow A: A Promising Therapeutic Agent for a Broad Spectrum of Diseases.Evidence-based complementary and alternative medicine : eCAM · 2018
    Review
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

11 authors at 3 institutions in 1 country.

Naping HuDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Jialin DuanDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Huihui LiDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Yanhua WangCollege of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang, 712046, China.
Fang WangDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Jianjie ChuDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Jin SunDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Meiyou LiuDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Chao WangDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Chengtao LuDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Aidong WenDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Air Force Medical University · CNXijing Hospital · CNShaanxi University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRenal fibrosis is the common pathological foundation of many chronic kidney diseases (CKDs). The aim of this study was to investigate whether Hydroxysafflor yellow A (HSYA) can preserve renal function by inhibiting the progression of renal fibrosis and the potential mechanisms.

methodsRenal fibrosis was induced by unilateral ureteral obstruction (UUO) performed on 7-week-old C57BL/6 mice. HSYA (10, 50 and 100 mg/kg) were intragastrically administered. Sham group and model group were administered with the same volume of vehicle. Serum and kidney samples were collected 14 days after the UUO surgery. Serum biochemical indicators were measured by automatic biochemical analyzer. Histological changes were evaluated by HE and Masson staining. In vitro, the anti-fibrotic effect of HSYA was tested on human recombinant transforming growth factor-β1 (TGF-β1) stimulated HK-2 cells. The protein levels of α-SMA, collagen-I and fibronectin in kidney tissue and HK-2 cells were measured by immunohistochemistry and immunofluorescence. The protein levels of apoptosis-relative and TGF-β1/Smad3 signaling were detected by western blot.

resultsHSYA slowed the development of renal fibrosis both in vivo and in vitro. In UUO rats, renal function index suggested that HSYA treatment decreased the level of serum creatinine (Scr) and blood urea nitrogen (BUN) rose by UUO (P<0.05). HE staining and Masson staining demonstrated that kidney interstitial fibrosis, tubular atrophy, and inflammatory cell infiltration were notably attenuated in the high-dose HSYA group compared with the model group. The expressions of α-SMA, collagen-I and fibronectin were decreased in the UUO kidney and HK-2 cells of the HSYA-treatment group. Moreover, HSYA reduced the apoptotic rate of HK-2 cells stimulated by TGF-β1. Further study revealed that HSYA regulated the TGF-β1/Smads signaling pathway both in kidney tissue and HK-2 cells.

conclusionsThese results suggested that HSYA had a protective effect against fibrosis in renal cells, at least partly, through inhibiting TGF-β1/smad3-mediated Epithelial-mesenchymal transition signaling pathway.

Indexed as

AnimalsApoptosisBlood Urea NitrogenCell ProliferationChalconeCreatinineDisease Models, AnimalEpithelial-Mesenchymal TransitionFibrosisKidneyKidney DiseasesMaleMice, Inbred C57BLQuinonesSmad3 ProteinTransforming Growth Factor beta1ChalconeCreatininehydroxysafflor yellow AQuinonesSmad3 ProteinSmad3 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID27088510
PMCPMC4835075
OpenAlexW2340790095

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.