Evidence map›Paper›PMID 23325452›Full record

ArticleNeurochemical research2013

Parecoxib suppresses CHOP and Foxo1 nuclear translocation, but increases GRP78 levels in a rat model of focal ischemia.

Zhi Ye, Na Wang, Pingping Xia, E Wang, Juan Liao, Qulian Guo

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  12. Interaction between CHOP and FoxO6 promotes hepatic lipid accumulation.Liver international : official journal of the International Association for the Study of the Liver · 2020
    Article
  13. Article
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  20. High molecular weight stress proteins: Identification, cloning and utilisation in cancer immunotherapy.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2013
    Review
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

6 authors at 2 institutions in 1 country.

Zhi YeDepartment of Anesthesiology, The Affiliated Xiangya Hospital of Central South University, Changsha, 410078 Hunan Province, China.
Na Wang
Pingping Xia
E Wang
Juan Liao
Qulian Guo
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parecoxib, a novel COX-2 inhibitor, functions as a neuroprotective agent and rescues neurons from cerebral ischemic reperfusion injury-induced apoptosis. However, the molecular mechanisms underlying parecoxib neuroprotection remain to be elucidated. There is growing evidence that endoplasmic reticulum (ER) stress plays an important role in neuronal death caused by brain ischemia. However, very little is known about the role of parecoxib in mediating pathophysiological reactions to ER stress induced by ischemic reperfusion injury. Therefore, in the present study, we investigated whether delayed administration of parecoxib attenuates brain damage via suppressing ER stress-induced cell death. Adult male Sprague-Dawley rats were administered parecoxib (10 or 30 mg kg(-1), IP) or isotonic saline twice a day starting 24 h after middle cerebral artery occlusion (MCAO) for three consecutive days. The expressions of glucose-regulated protein 78 (GRP78) and oxygen-regulated protein 150 (ORP150) and C/EBP-homologous protein (CHOP) and forkhead box protein O 1 (Foxo1) in cytoplasmic and nuclear fraction were determined by Western blotting. The levels of caspase-12 expression were checked by immunohistochemistry analysis, served as a marker for ER stress-induced apoptosis. Parecoxib significantly suppressed cerebral ischemic injury-induced nuclear translocation of CHOP and Foxo1 and attenuated the immunoreactivity of caspase-12 in ischemic penumbra. Furthermore, the protective effect of delayed administration of parecoxib was accompanied by an increased GRP78 and ORP150 expression. Therefore, our study suggested that elevation of GRP78 and ORP150, and suppression of CHOP and Foxo1 nuclear translocation may contribute to parecoxib-mediated neuroprotection during ER stress responses.

Indexed as

AnimalsApoptosisBrain IschemiaEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressForkhead Box Protein O1Forkhead Transcription FactorsHeat-Shock ProteinsHSP70 Heat-Shock ProteinsInfarction, Middle Cerebral ArteryIsoxazolesMaleNerve Tissue ProteinsNeuroprotective AgentsProteinsProtein TransportEndoplasmic Reticulum Chaperone BiPForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, ratGRP78 protein, ratHeat-Shock ProteinsHSP70 Heat-Shock ProteinsIsoxazolesNerve Tissue ProteinsNeuroprotective Agentsoxygen-regulated proteinsparecoxibProteinsTranscription Factor CHOP

Identifiers

PMID23325452
OpenAlexW2094666282

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.