Evidence map›Paper›PMID 26204831›Full record

ArticleInternational journal of molecular sciences2015

Baicalin Protects Mice from Aristolochic Acid I-Induced Kidney Injury by Induction of CYP1A through the Aromatic Hydrocarbon Receptor.

Ke Wang, Chenchen Feng, Chenggang Li, Jun Yao, Xiaofeng Xie, Likun Gong, Yang Luan, Guozhen Xing, Xue Zhu, Xinming Qi and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2015. 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
1.6field-weighted citation impact, top 18% 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.

  1. Review
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  10. Review
  11. Pharmacological blockage of the AHR-CYP1A1 axis: a call for in vivo evidence.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  12. Article
  13. Benzo[International journal of molecular sciences · 2021
    Article
  14. Article
  15. Review
  16. Aristolochic Acid Induces Chronic Kidney Disease in ACE Knockout Mice.International journal of preventive medicine · 2021
    Article
  17. Article
  18. Review
  19. Review
  20. Article
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 2 institutions in 1 country.

Ke WangKey Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi 214063, Jiangsu, China. wangke@jsinm.org.
Chenchen FengCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. shang320@hotmail.com.
Chenggang LiCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. lifen_888@hotmail.com.
Jun YaoCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. jyao@cdser.simm.ac.cn.
Xiaofeng XieCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. cluseee@gmail.com.
Likun GongCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. lkgong@cdser.simm.ac.cn.
Yang LuanCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. djlover@gmail.com.
Guozhen XingCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. gzxing@cdser.simm.ac.cn.
Xue ZhuKey Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi 214063, Jiangsu, China. zhuxue@jsinm.org.
Xinming QiCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. xmqi@cdser.simm.ac.cn.
Jin RenCenter for Drug Safety Evaluation and Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 201203, China. jren@cdser.simm.ac.cn.
Chinese Academy of Sciences · CNShanghai Institute of Materia Medica · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to aristolochic acid I (AAI) can lead to aristolochic acid nephropathy (AAN), Balkan endemic nephropathy (BEN) and urothelial cancer. The induction of hepatic CYP1A, especially CYP1A2, was considered to detoxify AAI so as to reduce its nephrotoxicity. We previously found that baicalin had the strong ability to induce CYP1A2 expression; therefore in this study, we examined the effects of baicalin on AAI toxicity, metabolism and disposition, as well as investigated the underlying mechanisms. Our toxicological studies showed that baicalin reduced the levels of blood urea nitrogen (BUN) and creatinine (CRE) in AAI-treated mice and attenuated renal injury induced by AAI. Pharmacokinetic analysis demonstrated that baicalin markedly decreased AUC of AAI in plasma and the content of AAI in liver and kidney. CYP1A induction assays showed that baicalin exposure significantly increased the hepatic expression of CYP1A1/2, which was completely abolished by inhibitors of the Aromatic hydrocarbon receptor (AhR), 3',4'-dimethoxyflavone and resveratrol, in vitro and in vivo, respectively. Moreover, the luciferase assays revealed that baicalin significantly increased the luciferase activity of the reporter gene incorporated with the Xenobiotic response elements recognized by AhR. In summary, baicalin significantly reduced the disposition of AAI and ameliorated AAI-induced kidney toxicity through AhR-dependent CYP1A1/2 induction in the liver.

Indexed as

Acute Kidney InjuryAnimalsAnti-Inflammatory Agents, Non-SteroidalAristolochic AcidsBalkan NephropathyCytochrome P-450 CYP1A1FlavonoidsHep G2 CellsHumansKidneyLiverMaleMiceMice, Inbred C57BLReceptors, Aryl HydrocarbonAnti-Inflammatory Agents, Non-Steroidalaristolochic acid IAristolochic AcidsbaicalinCytochrome P-450 CYP1A1FlavonoidsReceptors, Aryl Hydrocarbonaristolochic acidaromatic hydrocarbon receptorbaicalinCYP1Akidney injury

Identifiers

PMID26204831
PMCPMC4519959
OpenAlexW1508437190

What OpenQuestion holds

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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.