Evidence map›Paper›PMID 26300162›Full record

ArticleInternational urology and nephrology2015

Protective effects of edaravone, a free radical scavenger, on lipopolysaccharide-induced acute kidney injury in a rat model of sepsis.

Lin Liu, Yijin Song, Ming Zhao, Zhuwen Yi, Qiyi Zeng

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Article in International urology and nephrology, 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
2.3field-weighted citation impact, top 14% 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, 48 citations in OpenAlex.

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  18. Neuronal Mitochondria Modulation of LPS-Induced Neuroinflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  19. Article
  20. 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

5 authors at 3 institutions in 1 country.

Lin LiuDepartment of Pediatry, The Third Xiangya Hospital of Central South University, Changsha, 410013, Hunan, China.
Yijin SongDivision of Pediatric Nephrology Pediatric Medical Center, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Ming ZhaoDepartment of Pediatry, The Third Xiangya Hospital of Central South University, Changsha, 410013, Hunan, China.
Zhuwen YiDivision of Pediatric Nephrology Pediatric Medical Center, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China. yizhuwen1969@163.com.
Qiyi ZengDepartment of Pediatrics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, 510280, P.R. China. zqy_88@163.com.
Central South University · CNSouthern Medical University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAcute kidney injury (AKI) is a frequent complication of sepsis. The present work examined the therapeutic potential of edaravone (EDA), a free radical scavenger, for inhibiting sepsis-induced renal injury.

methodsSaline and lipopolysaccharide (LPS) were injected intraperitoneally at a dose of 10 mg/kg of body weight. EDA, 3-methyl-1-phenyl-pyrazolin-5-one, was administrated intravenously at a dose of 3 mg/kg of body weight to male Wistar rats. Wistar rats were divided into four groups: treatment with LPS alone, treatment with LPS followed by EDA administration, treatment with saline followed by EDA administration, and untreated controls.

resultsAdministration of LPS caused a significant increase in BUN and serum creatinine levels with concurrent pathological alterations in kidney tissues. EDA treatment relieved all these changes. Moreover, EDA reduced LPS-induced elevation of serum TNF-α and IL-6 in rats. Furthermore, EDA could prevent mitochondrial membrane potential loss induced by LPS and reverse the changes in mitochondrial antioxidant (such as T-AOC, SOD, CAT, and GSH) and mitochondrial MDA levels. TUNEL staining of the kidney sections and immunoblot analysis on renal cortical lysates showed that EDA treatment resulted in reduced number of apoptotic cells, which occurred concomitantly with decreased levels of cytochrome c and cleaved caspase 3. Following LPS treatment of rat renal tubular cells, mitochondrial fragmentation was observed prior to apoptosis, which was inhibited by EDA.

conclusionsEDA prevents LPS-induced AKI not only by reducing the production of inflammatory cytokines, but also by attenuating oxidative damage in renal mitochondria, mitochondrial fragmentation, and apoptosis of renal cells.

Indexed as

Acute Kidney InjuryAnimalsAntipyrineApoptosisBlood Urea NitrogenCatalaseCells, CulturedDisease Models, AnimalEdaravoneFree Radical ScavengersGlutathioneInterleukin-6Kidney TubulesLipopolysaccharidesMaleMalondialdehydeAntipyrineCatalaseEdaravoneFree Radical ScavengersGlutathioneInterleukin-6LipopolysaccharidesMalondialdehydeSuperoxide DismutaseTumor Necrosis Factor-alphaAcute kidney injuryEdaravoneLPSMitochondrial fragmentationSepsis

Identifiers

PMID26300162
OpenAlexW1152340322

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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.