Evidence map›Paper›PMID 24559268›Full record

ArticleJournal of translational medicine2014

Delayed treatment with oleanolic acid attenuates tubulointerstitial fibrosis in chronic cyclosporine nephropathy through Nrf2/HO-1 signaling.

Yu Ah Hong, Ji Hee Lim, Min Young Kim, Eun Nim Kim, Eun Sil Koh, Seok Joon Shin, Bum Soon Choi, Cheol Whee Park, Yoon Sik Chang, Sungjin Chung

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 12% 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, 48 citations in OpenAlex.

  1. Review
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  6. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021
    Review
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  8. Toxicology reports · 2021
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  18. Heme Oxygenase-1 in Kidney Health and Disease.Antioxidants & redox signaling · 2016
    Review
  19. Article
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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

10 authors at 3 institutions in 1 country.

Yu Ah Hong
Ji Hee Lim
Min Young Kim
Eun Nim Kim
Eun Sil Koh
Seok Joon Shin
Bum Soon Choi
Cheol Whee Park
Yoon Sik Chang
Sungjin ChungDepartment of Internal Medicine, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seoul 137-701, Republic of Korea. sungjin.chung@outlook.com.
Catholic University of Korea · KRKorea University Medical Center · KRSeoul St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNuclear factor erythroid-2-related factor-2 (Nrf2) is known to protect against tissue injury by orchestrating antioxidant and detoxification responses to oxidative stress. This study investigated whether upregulation of Nrf2-dependent signaling by oleanolic acid (OA), which is known to activate Nrf2, could attenuate renal inflammation and fibrosis in cyclosporine (CsA)-induced kidney injury.

methodsMale ICR mice were divided into four treatment groups: Vehicle (VH, n = 6), VH + OA (n = 6), CsA (n = 8), and CsA + OA (n = 8). For the OA-treated groups, OA (25 mg/kg/day) was administered by intraperitoneal injection for the final week of the 4-week experimental period. Renal function, morphologies and signaling were evaluated at the end of the study.

resultsTreatment with CsA resulted in decreased kidney function and urine osmolality and increased urine volume and urinary albumin levels. The CsA-induced changes were improved by OA treatment. Specifically, administration of OA decreased tubulointerstitial fibrosis and inflammation scores that were increased in CsA-treated mice. Furthermore, OA treatment decreased urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-epi-prostaglandin F2α (8-iso-PGF2α) levels. The beneficial effects of OA were attributed to an increased ratio of nuclear/total Nrf2 and subsequently enhanced expression of heme oxygenase (HO)-1, as well as a stable level of Kelch-like ECH-associated protein 1 (Keap1) expression, indicating that OA enhanced nuclear translocation of Nrf2. Increased apoptotic cell death and a high ratio of B cell leukaemia/lymphoma 2 (Bcl-2)-associated X protein (Bax) to Bcl-2 in CsA-treated mice were also significantly ameliorated by OA treatment.

conclusionOur results suggest that OA activates Nrf2/HO-1 signaling in chronic CsA nephropathy, which may have beneficial effects on inflammation and oxidative stress.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntioxidantsApoptosisBiomarkersCell NucleusCyclosporineCytoskeletal ProteinsFibrosisHeme Oxygenase-1Kelch-Like ECH-Associated Protein 1Kidney DiseasesKidney Function TestsKidney TubulesMaleMalondialdehydeAdaptor Proteins, Signal TransducingAntioxidantsBiomarkersCyclosporineCytoskeletal ProteinsHeme Oxygenase-1Keap1 protein, mouseKelch-Like ECH-Associated Protein 1MalondialdehydeNAD(P)H Dehydrogenase (Quinone)NF-E2-Related Factor 2Nqo1 protein, mouseOleanolic AcidProto-Oncogene Proteins c-bcl-2

Identifiers

PMID24559268
PMCPMC3939938
OpenAlexW2120416165

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.