Evidence map›Paper›PMID 26261486›Full record

ArticleInternational journal of clinical and experimental pathology2015

Astaxanthin improves cognitive deficits from oxidative stress, nitric oxide synthase and inflammation through upregulation of PI3K/Akt in diabetes rat.

Lianbao Xu, Juan Zhu, Weibing Yin, Xinsheng Ding

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 82 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

4 authors at 2 institutions in 1 country.

Lianbao XuDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, China ; Department of Neurology, Suqian People's Hospital of Nanjing Drum Tower Hospital Group Suqian, 223800, China.
Juan ZhuDepartment of Pediatrics, Suqian People's Hospital of Nanjing Drum Tower Hospital Group Suqian, 223800, China.
Weibing YinDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, China.
Xinsheng DingDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, China.
Jiangsu Province Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes-induced cognitive deficit (DICD) is a prevalent disease with substantial morbidity and mortality and as a global health problem with serious economic burdens. Astaxanthin (AST) has a good prospect in production of nutritional, medical, and particularly functional health drug. The present study was aimed to study the effect of AST on DICD in diabetes mellitus (DM) rat through suppression of oxidative stress, nitric oxide synthase (NOS) pathway, inflammatory reaction and upregulation of PI3K/Akt. In the study, Morris water maze teat was used to detect the cognitive function of DM rat. Afterwards, we measured the body weight and blood glucose levels of DM rats. Then, oxidative stress, the activities of eNOS and iNOS, and inflammatory factors were analyzed using a commercial kit in cerebral cortex and hippocampus. Finally, the caspase-3/9 and phosphoinositide 3-kinase (PI3K)/Akt expressions were also checkout with Real Time PCR and immunoblotting, respectively. In this experiment, AST could availably enhance the body weight and reduce blood glucose levels of DM rats. Moreover, AST could observably perfect cognitive function of DM rat. Next, the activities of oxidative stress, nitric oxide synthase and inflammation were distinctly diminution in DM rat, after the treatment of AST. Furthermore, our present results demonstrated that AST had the protective effect on the brain cell of DM rat, decreased the caspase-3/9 expression and promoted the expression of PI3K/Akt in cerebral cortex and hippocampus.

Indexed as

AnimalsAnti-Inflammatory AgentsAntioxidantsBlood GlucoseBody WeightBrainCaspase 3Caspase 9CognitionCognition DisordersDiabetes Mellitus, ExperimentalInflammationInflammation MediatorsMaleNitric Oxide SynthaseNitric Oxide Synthase Type IIAnti-Inflammatory AgentsAntioxidantsastaxanthineBlood GlucoseCasp3 protein, ratCasp9 protein, ratCaspase 3Caspase 9Inflammation MediatorsNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, ratNos3 protein, ratPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktXanthophyllsastaxanthinDiabetes-induced cognitive deficitinflammatorynitric oxide synthaseoxidative stressPI3K/Akt

Identifiers

PMID26261486
PMCPMC4525820
OpenAlexW2400832068

What OpenQuestion holds

Textmetadata
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.