Evidence map›Paper›PMID 32492962›Full record

ArticleCells2020

Effects of β-Adrenergic Blockade on Metabolic and Inflammatory Responses in a Rat Model of Ischemic Stroke.

Shih-Yi Lin, Ya-Yu Wang, Cheng-Yi Chang, Chih-Cheng Wu, Wen-Ying Chen, Yu-Hsiang Kuan, Su-Lan Liao, Chun-Jung Chen

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  7. Neuroprotective effects of phenylacetylglycine via β2AR on cerebral ischemia/reperfusion injury in rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
    Article
  8. Pulsed electromagnetic fields inhibit IL-37 to alleviate CD8Apoptosis : an international journal on programmed cell death · 2024
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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 7 institutions in 1 country.

Shih-Yi LinCenter for Geriatrics and Gerontology, Taichung Veterans General Hospital, Taichung City 407, Taiwan.ORCID 0000-0002-1901-2656
Ya-Yu WangInstitute of Clinical Medicine, National Yang Ming University, Taipei City 112, Taiwan.
Cheng-Yi ChangDepartment of Surgery, Feng Yuan Hospital, Taichung City 420, Taiwan.
Chih-Cheng WuDepartment of Anesthesiology, Taichung Veterans General Hospital, Taichung City 407, Taiwan.
Wen-Ying ChenDepartment of Veterinary Medicine, National Chung-Hsing University, Taichung City 402, Taiwan.
Yu-Hsiang KuanDepartment of Pharmacology, Chung Shan Medical University, Taichung City 402, Taiwan.
Su-Lan LiaoDepartment of Medical Research, Taichung Veterans General Hospital, Taichung City 407, Taiwan.
Chun-Jung ChenDepartment of Medical Research, Taichung Veterans General Hospital, Taichung City 407, Taiwan.
National Yang Ming Chiao Tung University · TWChina Medical University · TWChung Shan Medical University · TWNational Chung Hsing University · TWProvidence University · TWTaichung Hospital · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke provokes an inflammatory response concurrent with both sympathetic nervous system activation and hyperglycemia. Currently, their crosstalk and consequences in stroke outcomes are of clinical attraction. We have provided experimental evidence showing the suppressive effects of the nonselective β-adrenoreceptor antagonist propranolol on hyperglycemia, inflammation, and brain injury in a rat model experiencing cerebral ischemia. Pretreatment with propranolol protected against postischemic brain infarction, edema, and apoptosis. The neuroprotection caused by propranolol was accompanied by a reduction in fasting glucose, fasting insulin, glucose tolerance impairment, plasma C-reactive protein, plasma free fatty acids, plasma corticosterone, brain oxidative stress, and brain inflammation. Pretreatment with insulin alleviated-while glucose augmented-postischemic brain injury and inflammation. Additionally, the impairment of insulin signaling in the gastrocnemius muscles was noted in rats with cerebral ischemia, with propranolol improving the impairment by reducing oxidative stress and tumor necrosis factor-α signaling. The anti-inflammatory effects of propranolol were further demonstrated in isoproterenol-stimulated BV2 and RAW264.7 cells through its ability to decrease cytokine production. Despite their potential benefits, stroke-associated hyperglycemia and inflammation are commonly linked with harmful consequences. Our findings provide new insight into the anti-inflammatory, neuroprotective, and hypoglycemic mechanisms of propranolol in combating neurodegenerative diseases, such as stroke.

Indexed as

Adrenergic beta-AntagonistsAnimalsBrain InjuriesCell LineCytokinesDisease Models, AnimalGlucoseHyperglycemiaInflammationInsulinIschemic StrokeIsoproterenolMaleMiceMusclesNeuroprotectionAdrenergic beta-AntagonistsCytokinesGlucoseInsulinIsoproterenolNeuroprotective AgentsPropranololadrenergic systemmicroglia polarizationneuroinflammationstroke

Identifiers

PMID32492962
PMCPMC7349353
OpenAlexW3030606698

What Socratic holds

Textmetadata
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 Socratic graph.