Evidence map›Paper›PMID 28565857›Full record

ArticleExperimental and therapeutic medicine2017

Role of the PI3K/AKT signalling pathway in apoptotic cell death in the cerebral cortex of streptozotocin-induced diabetic rats.

Yan Meng, Weiwei Wang, Jinsong Kang, Xinxue Wang, Liankun Sun

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 80 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

5 authors at 1 institution in 1 country.

Yan MengDepartment of Pathophysiology, Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Weiwei WangDepartment of Pathophysiology, Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Jinsong KangDepartment of Pathophysiology, Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Xinxue WangDepartment of Pathophysiology, Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Liankun SunDepartment of Pathophysiology, Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus is associated with cognitive dysfunction. Numerous previous studies have shown that type 1 diabetes-induced hyperglycaemia causes structural brain damage, such as a decrease in whole-brain grey matter. The impact of diabetes mellitus on the cerebral cortex is poorly understood and requires further clarification. In the present study, diabetes was induced via an intraperitoneal injection of streptozotocin (50 mg/kg). Hematoxylin and eosin (H&E) staining was performed to detect the morphological changes in the cerebral cortex, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining was used to detect neuronal apoptosis and western blotting was performed to determine protein expression levels. Nine weeks after the induction of diabetes, the body weight was significantly lower and the blood glucose levels were significantly higher in the diabetic rats than in the control rats (P<0.05). H&E staining revealed nuclear chromatin condensation and cytoplasmic shrinkage in the cerebral cortex of the diabetic rats and TUNEL staining further indicated apoptotic changes in the cerebral cortex of the diabetic rats. The ratio of B-cell lymphoma 2 (Bcl-2) -associated X protein/Bcl-2 and the expression of cytochrome c and activated caspase-3 (cleaved caspase-3) were significantly increased, whereas the ratio of phosphorylated AKT/AKT was significantly decreased in the diabetic rats compared with that in the control rats (P<0.05). Taken together, these results suggested that diabetes mellitus may induce neuronal apoptosis in the cerebral cortex by downregulating AKT phosphorylation.

Indexed as

AKTapoptosisBaxBcl-2cerebral cortexdiabetes mellitusstreptozotocin

Identifiers

PMID28565857
PMCPMC5443277
OpenAlexW2603452325

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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.