Evidence map›Paper›PMID 26379247›Full record

ArticlePloS one2015

A Mitochondrion-Targeted Antioxidant Ameliorates Isoflurane-Induced Cognitive Deficits in Aging Mice.

Jing Wu, Huihui Li, Xiaoru Sun, Hui Zhang, Shuangying Hao, Muhuo Ji, Jianjun Yang, Kuanyu Li

Open access · goldAbstract read
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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 53 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

8 authors at 2 institutions in 1 country.

Jing WuJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, China; Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Huihui LiJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, China.
Xiaoru SunDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Hui ZhangDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Shuangying HaoJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, China.
Muhuo JiDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Jianjun YangDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Kuanyu LiJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, China.
Nanjing University · CNNanjing General Hospital of Nanjing Military Command · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isoflurane possesses neurotoxicity and can induce cognitive deficits, particularly in aging mammals. Mitochondrial reactive oxygen species (mtROS) have been linked to the early pathogenesis of this disorder. However, the role of mtROS remains to be evaluated due to a lack of targeted method to treat mtROS. Here, we determined in aging mice the effects of the mitochondrion-targeted antioxidant SS-31, on cognitive deficits induced by isoflurane, a general inhalation anesthetic. We further investigated the possible mechanisms underlying the effects of SS-31 on hippocampal neuro-inflammation and apoptosis. The results showed that isoflurane induced hippocampus-dependent memory deficit, which was associated with mitochondrial dysfunction including reduced ATP contents, increased ROS levels, and mitochondrial swelling. Treatment with SS-31 significantly ameliorated isoflurane-induced cognitive deficits through the improvement of mitochondrial integrity and function. Mechanistically, SS-31 treatment suppressed pro-inflammatory responses by decreasing the levels of NF-κB, NLRP3, caspase 1, IL-1β, and TNF-α; and inhibited the apoptotic pathway by decreasing the Bax/Bcl-2 ratio, reducing the release of cytochrome C, and blocking the cleavage of caspase 3. Our results indicate that isoflurane-induced cognitive deficits may be attenuated by mitochondrion-targeted antioxidants, such as SS-31. Therefore, SS-31 may have therapeutic potentials in preventing injuries from oxidative stresses that contribute to anesthetic-induced neurotoxicity.

Indexed as

AgingAdenosine TriphosphateAnesthetics, InhalationAnimalsAntioxidantsCognition DisordersIsofluraneMaleMiceMice, Inbred C57BLMitochondriaReactive Oxygen SpeciesAdenosine TriphosphateAnesthetics, InhalationAntioxidantsIsofluraneReactive Oxygen Species

Identifiers

PMID26379247
PMCPMC4575031
OpenAlexW2199760645

What OpenQuestion holds

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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.