Evidence map›Paper›PMID 25761053›Full record

ArticlePloS one2015

Protective effects of astaxanthin on ConA-induced autoimmune hepatitis by the JNK/p-JNK pathway-mediated inhibition of autophagy and apoptosis.

Jingjing Li, Yujing Xia, Tong Liu, Junshan Wang, Weiqi Dai, Fan Wang, Yuanyuan Zheng, Kan Chen, Sainan Li, Huerxidan Abudumijiti and 12 more

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

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
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  5. Targeting GPR84 to alleviate acute immune-mediated liver injury.Molecular medicine (Cambridge, Mass.) · 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

22 authors at 3 institutions in 1 country.

Jingjing LiDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yujing XiaDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Tong LiuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Junshan WangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Weiqi DaiDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Fan WangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yuanyuan ZhengDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Kan ChenDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Sainan LiDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Huerxidan AbudumijitiDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Zheng ZhouDepartment of Gastroenterology, Shanghai Tenth People's Hospital, The First Clinical Medical College of Nanjing Medical University, Nanjing, 210029, China.
Jianrong WangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, The First Clinical Medical College of Nanjing Medical University, Nanjing, 210029, China.
Wenxia LuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, The First Clinical Medical College of Nanjing Medical University, Nanjing, 210029, China.
Rong ZhuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, The First Clinical Medical College of Nanjing Medical University, Nanjing, 210029, China.
Jing YangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Huawei ZhangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Soochow University, Suzhou, 215006, China.
Qin YinDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Soochow University, Suzhou, 215006, China.
Chengfen WangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yuqing ZhouDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Soochow University, Suzhou, 215006, China.
Jie LuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yingqun ZhouDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Chuanyong GuoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Tongji University · CNShanghai Tenth People's Hospital · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAstaxanthin, a potent antioxidant, exhibits a wide range of biological activities, including antioxidant, atherosclerosis and antitumor activities. However, its effect on concanavalin A (ConA)-induced autoimmune hepatitis remains unclear. The aim of this study was to investigate the protective effects of astaxanthin on ConA-induced hepatitis in mice, and to elucidate the mechanisms of regulation. MATERIALS AND

methodsAutoimmune hepatitis was induced in in Balb/C mice using ConA (25 mg/kg), and astaxanthin was orally administered daily at two doses (20 mg/kg and 40 mg/kg) for 14 days before ConA injection. Levels of serum liver enzymes and the histopathology of inflammatory cytokines and other maker proteins were determined at three time points (2, 8 and 24 h). Primary hepatocytes were pretreated with astaxanthin (80 μM) in vitro 24 h before stimulation with TNF-α (10 ng/ml). The apoptosis rate and related protein expression were determined 24 h after the administration of TNF-α.

resultsAstaxanthin attenuated serum liver enzymes and pathological damage by reducing the release of inflammatory factors. It performed anti-apoptotic effects via the descending phosphorylation of Bcl-2 through the down-regulation of the JNK/p-JNK pathway.

conclusionThis research firstly expounded that astaxanthin reduced immune liver injury in ConA-induced autoimmune hepatitis. The mode of action appears to be downregulation of JNK/p-JNK-mediated apoptosis and autophagy.

Indexed as

Administration, OralAnimalsApoptosisAutophagyCells, CulturedConcanavalin ACytokinesDrug Administration ScheduleHepatitis, AutoimmuneHepatocytesLiverMAP Kinase Signaling SystemMiceMice, Inbred BALB CXanthophyllsastaxanthineConcanavalin ACytokinesXanthophylls

Identifiers

PMID25761053
PMCPMC4356569
OpenAlexW2094058775

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.