Evidence map›Paper›PMID 25815309›Full record

ArticleBioMed research international2015

Lutein has a protective effect on hepatotoxicity induced by arsenic via Nrf2 signaling.

Shugang Li, Yusong Ding, Qiang Niu, Shangzhi Xu, Lijuan Pang, Rulin Ma, Mingxia Jing, Gangling Feng, Jing Xia Tang, Qian Zhang and 7 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 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

17 authors at 2 institutions in 1 country.

Shugang LiDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Yusong DingDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Qiang NiuDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Shangzhi XuDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Lijuan PangDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi, Xinjiang 832002, China.
Rulin MaDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Mingxia JingDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Gangling FengDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Jing Xia TangDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Qian ZhangDepartment of Science and Technology, The Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi 830011, China.
Xiaomei MaDepartment of Pathology, The Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi 830011, China.
Yizhong YanDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Jingyu ZhangDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.ORCID 0000-0002-2492-6743
Meng WeiDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.ORCID 0000-0001-5451-3125
Hai Xia WangDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Feng LiDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi, Xinjiang 832002, China.
Shuxia GuoDepartment of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China.
Shihezi University · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arsenic produces liver disease through the oxidative stress. While lutein can alleviate cytotoxic and oxidative injury, nuclear factor erythroid 2-related factor 2 (Nrf2) pathway plays a critical role in defending oxidative species. However, the mechanisms by which lutein protects the liver against the effect of arsenic are not known. Therefore, this study aims to investigate the mechanisms involved in the action of lutein using mice model in which hepatotoxicity was induced by arsenic. We found that mice treatment with lutein could reverse changes in morphological and liver indexes and result in a significant improvement in hepatic function comparing with arsenic trioxide group. Lutein treatment improved the activities of antioxidant enzymes and attenuated increasing of ROS and MDA induced by arsenic trioxide. Lutein could increase the mRNA and protein expression of Nrf2 signaling related genes (Nrf2, Nqo1, Ho-1, and Gst). These findings provide additional evidence that lutein may be useful for reducing reproductive injury associated with oxidative stress by the activation of Nrf2 signaling. Our findings suggest a possible mechanism of antioxidant lutein in preventing the hepatotoxicity, which implicate that a dietary lutein may be a potential treatment for liver diseases, especially for arsenicosis therapy.

Indexed as

AnimalsAntioxidantsArsenicArsenicalsArsenic TrioxideBlotting, WesternFemaleGene Expression RegulationGlutathioneImmunohistochemistryLiverLuteinMaleMalondialdehydeMiceNF-E2-Related Factor 2AntioxidantsArsenicArsenicalsArsenic TrioxideGlutathioneLuteinMalondialdehydeNF-E2-Related Factor 2OxidesProtective AgentsSuperoxide Dismutase

Identifiers

PMID25815309
PMCPMC4357133
OpenAlexW2076212359

What OpenQuestion holds

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LicenceCC BY
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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.