Evidence map›Paper›PMID 29171428›Full record

ArticleNeural regeneration research2017

The role of glycogen synthase kinase 3 beta in brain injury induced by myocardial ischemia/reperfusion injury in a rat model of diabetes mellitus.

Bo Zhao, Wen-Wei Gao, Ya-Jing Liu, Meng Jiang, Lian Liu, Quan Yuan, Jia-Bao Hou, Zhong-Yuan Xia

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. LncRNA KCNQ1OT1 aggravates myocardial ischemia/reperfusion injury by mediating the EZH2/TIMP-3 axis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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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.

Bo ZhaoDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Wen-Wei GaoDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Ya-Jing LiuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Meng JiangDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Lian LiuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Quan YuanDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Jia-Bao HouDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Zhong-Yuan XiaDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischemia/reperfusion injury can lead to severe brain injury. Glycogen synthase kinase 3 beta is known to be involved in myo-cardial ischemia/reperfusion injury and diabetes mellitus. However, the precise role of glycogen synthase kinase 3 beta in myocardial ischemia/reperfusion injury-induced brain injury is unclear. In this study, we observed the effects of glycogen synthase kinase 3 beta on brain injury induced by myocardial ischemia/reperfusion injury in diabetic rats. Rat models of diabetes mellitus were generated via intraperitoneal injection of streptozotocin. Models of myocardial ischemia/reperfusion injury were generated by occluding the anterior descending branch of the left coronary artery. Post-conditioning comprised three cycles of ischemia/reperfusion. Immunohistochemical staining and western blot assays demonstrated that after 48 hours of reperfusion, the structure of the brain was seriously damaged in the experimental rats compared with normal controls. Expression of Bax, interleukin-6, interleukin-8, terminal deoxynucleotidyl transferase dUTP nick end labeling, and cleaved caspase-3 in the brain was significantly increased, while expression of Bcl-2, interleukin-10, and phospho-glycogen synthase kinase 3 beta was decreased. Diabetes mellitus can aggravate inflammatory reactions and apoptosis. Ischemic post-conditioning with glycogen synthase kinase 3 beta inhibitor lithium chloride can effectively reverse these changes. Our results showed that myocardial ischemic post-conditioning attenuated myocardial ischemia/reperfusion injury-induced brain injury by activating glyco-gen synthase kinase 3 beta. According to these results, glycogen synthase kinase 3 beta appears to be an important factor in brain injury induced by myocardial ischemia/reperfusion injury.

Indexed as

brain injurydiabetes mellitusglycogen synthase kinase 3 betaischemic post-conditioningmyocardial ischemia/reperfusion injurynerve regenerationneural regeneration

Identifiers

PMID29171428
PMCPMC5696844
OpenAlexW2766525784

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.